Ischemic heart disease remains the leading cause of global disease burden among cardiovascular disorders. In addition to cardiomyocyte injury, ischemia-reperfusion (I/R)-induced microvascular damage plays a crucial role in determining tissue dysfunction and overall prognosis. Mitochondria-associated endoplasmic reticulum membranes (MAMs), specialized contact sites between the ER and mitochondria, are now recognized as key regulators of cardiovascular pathophysiology. The present review summarized current knowledge of the structure of MAMs and their effects on endothelial cells under hypoxia/reoxygenation conditions. Particular attention was given to their role in regulating mitochondrial quality control processes, including fission, fusion, oxidative stress, mitophagy and Ca2+ homeostasis, within the context of cardiac microvascular I/R injury. Targeting MAMs may represent a promising strategy for microvascular protection in ischemic heart disease.

Branched‑chain amino acids (BCAAs) are biologically active amino acids with branched carbon chains, recognized for their diverse biological functions and therapeutic potential. BCAAs have demonstrated promising effects in the prevention and treatment of various conditions, including muscle growth disorders, cardiovascular diseases and cancer. Despite extensive research confirming their targeted therapeutic effects in multiple domains, the mechanisms of action and therapeutic range of BCAAs remain incompletely understood. Osteoporosis, a metabolic bone disease, is a global public health issue characterized by an imbalance between osteoblast‑mediated bone formation and osteoclast‑induced bone resorption, resulting in fragile bones and an elevated risk of fractures. Given the well‑documented therapeutic roles of BCAAs, their potential link to osteoporosis has been explored, emphasizing the influence of BCAA metabolism on bone metabolism. The present review aims to summarize findings on the relationship between BCAA metabolism and osteoporosis, and to investigate the mechanisms by which BCAA metabolism may exert anti‑osteoporotic effects. The review first outlines the fundamental processes and key factors influencing bone metabolism, BCAA metabolism and osteoporosis. It then examines the interactions between these processes and the effects of BCAA metabolism on bone health. Finally, it explores the potential of targeting BCAA metabolic pathways as a future therapeutic strategy for osteoporosis, highlighting BCAAs as a promising target for treating this condition.

Long‑term hyperglycemia can damage the capillaries and neural regulation of the lungs, leading to pulmonary microvascular disease and neural regulation disorders, causing abnormalities in lung structure and function. The present study explored the effect of fibroblast growth factor (FGF)4 as a potential therapeutic growth factor on the effect of hyperglycemia on the lungs and models. The effect of FGF4 on the damage of lung cells caused by high glucose was evaluated and by a series of biochemical experiments (indirect immunofluorescence, western blotting, immunohistochemistry and siRNA). The results showed that FGF4 could effectively alleviate the inhibition of lung cell proliferation caused by high glucose. Further experiments found that high glucose caused inflammation, oxidative stress and fibrosis of lung cells, while the above pathological reactions were alleviated after treatment with FGF4. Further mechanism research showed that FGF4 treatment could markedly improve the survival rate of lung cells, reduce cell death and inflammatory responses and enhance the antioxidant stress resistance of cells. These effects are achieved by activating the adenosine monophosphate (AMP)‑activated protein kinase (AMPK)‑peroxisome proliferator‑activated receptor coactivator 1 (PGC‑1) signaling axis, which plays an important role in regulating cellular metabolism, antioxidant stress and anti‑inflammatory responses. experiments further confirmed the mitigating effect of FGF4 on lung tissue damage caused by high glucose. FGF4 treatment to diabetic model animals, lung function can be markedly improved and the degree of lung inflammation and fibrosis can be reduced. In summary, FGF4 exhibits a significant mitigating effect on high‑glucose‑induced lung cell damage through the AMPK‑PGC‑1 signaling axis, providing a new strategy for the treatment of diabetes and its pulmonary complications.

Endometriosis is a complex, chronic inflammatory gynecological disorder with estrogen‑dependent characteristics that severely impairs the quality of life of women and potentially leads to infertility. However, its pathogenesis remains poorly understood. Exosomes, small, discoid vesicles released by nearly all cell types, serve essential functions in multiple biological processes, including immune evasion, cellular migration, and differentiation. These vesicles can transport a broad repertoire of bioactive molecules, cross cell membranes readily, and remain stable within cells and body fluids. The present review summarizes global research from the last two decades on the mechanistic associations between exosomes and endometriosis, emphasizing their potential as vehicles for therapeutic delivery. Notably, the biological hallmarks of endometriosis such as fibrosis, immune dysregulation, angiogenesis, and aberrant cellular proliferation and migration, align with exosomal functions, suggesting that exosomes may contribute to disease progression. Furthermore, the use of exosomes as natural carriers for endometriosis treatment has been proposed, suggesting novel therapeutic avenues.

Glioblastoma (GBM) is the most aggressive primary malignant brain tumor type in adults, and is characterized by high invasiveness, therapeutic resistance and recurrence. Current treatments, primarily surgery combined with radiotherapy and chemotherapy, offer limited efficacy, thus necessitating more effective interventions. Matrix metalloproteinases (MMPs) crucially contribute to GBM progression through extracellular matrix degradation, epithelial‑mesenchymal transition and angiogenesis. MMP expression is intricately regulated by signaling pathways, non‑coding RNAs and the tumor microenvironment. Recently, strategies targeting MMPs have gained attention, including natural active substances and small‑molecule compounds with promising therapeutic potential. Nano‑delivery systems have notably improved drug delivery efficiency to the brain by overcoming the blood‑brain barrier, and combination therapies have demonstrated enhanced efficacy. However, chemotherapy resistance and functional heterogeneity remain critical challenges. The present review summarizes recent advances in understanding MMP regulatory mechanisms in GBM, highlighting the roles of signaling pathways and non‑coding RNAs. Additionally, the therapeutic potential of natural products, small‑molecule inhibitors, smart nanocarriers and combination treatments are discussed. Future research should focus on identifying novel inhibitors, and leveraging interdisciplinary approaches to facilitate precision‑targeted drug development, thereby addressing current treatment bottlenecks in GBM.

Emerging evidence from our prior investigations has elucidated the dose-dependent regulatory effects of low-dose ionizing radiation on cellular behaviors including proliferation, migration and differentiation in HLE-B3 lens epithelial cells, with concomitant activation of the canonical Wnt/β-catenin signaling cascade. To extend these findings to alternative cellular models, the present study systematically evaluated the biological responses of the well-characterized human lens epithelial cell line SRA01/04 to low-dose ionizing radiation exposure (0.05-0.2 Gy) versus high-dose radiation (0.5-2 Gy), with particular emphasis on temporal dynamics during acute (0-72 h) and chronic (7 days) phases. Mechanistically, lentivirus-mediated RNA interference was employed to establish stable High mobility group box protein 1 (HMGB1)-knockdown cell models, enabling rigorous interrogation of β-catenin subcellular localization and functional readouts under 0, 0.1 and 0.2 Gy γ-ray exposures. Key findings revealed the following: i) low-dose ionizing radiation within the 0.05-0.2 Gy range significantly potentiated SRA01/04 cell proliferation and migration capacity (P<0.05), concomitant with nuclear accumulation of β-catenin; ii) genetic ablation of HMGB1 abolished radiation-induced β-catenin nuclear translocation, resulting in 77% reduction in proliferation rate and 82% suppression of migratory activity compared with wild-type counterparts under equivalent radiation. The experimental evidence identifies HMGB1-mediated signaling as the critical molecular nexus connecting low-dose ionizing radiation exposure to dysregulated Wnt/β-catenin activity in lens epithelium, offering a new therapeutic target for preventing radiation-related cataracts.

Macrophages play a key role in hepatocellular carcinoma (HCC) progression, but the mechanisms underlying this involvement remain unclear. In the present study, mice with HCC were used for experiments, and 97H and THP‑1 cells were used for experiments. Metabolomic analysis was performed to detect changes of metabolites in the supernatant of 97H cells. Flow cytometry and immunohistochemical staining were performed to assess macrophage polarization. Western blotting was performed to examine the levels of phosphorylated (p‑) PI3K, p‑AKT and NRF2. Reverse transcription‑quantitative polymerase chain reaction was performed to examine , and mRNA expression levels. FBXO22 significantly promoted the release of myo‑inositol in the cell supernatant of 97H cells, markedly decreased the number of CD86‑positive cells (M1 macrophages), and increased the number of CD206‑positive cells (M2 macrophages) in both THP‑1 cells and mouse HCC tumor tissues. The promoting effect of myo‑inositol on M2 macrophages was reversed by transfection with small interfering (si)‑SLC5A3 . In addition, FBXO22 overexpression reduced PTEN protein levels and then elevated NRF2 protein levels upregulating IMPA1 and inducing myo‑inositol release in 97H cells. Co‑culturing of 97H and THP‑1 cells revealed that the stimulatory effect of 97H cells transfected with an overexpression (oe)‑ construct on M2 macrophages was reversed by co‑transfection with the si‑. Co‑immunoprecipitation revealed a promoting effect of FBXO22 on PTEN ubiquitination via direct interaction in 97H cells. Furthermore, luciferase activity and chromatin immunoprecipitation assays indicated direct transcriptional regulation of IMPA1 expression by NRF2 in 97H cells. The experiments further revealed that transfection with the si‑ reversed the promoting effect of oe‑ on tumor growth and M2 polarization by reducing myo‑inositol levels in tumor tissues. In conclusion, FBXO22 degrades PTEN by inducing its ubiquitination to elevate NRF2 protein levels. As a result, IMPA1 expression is increased, which causes myo‑inositol release by HCC cells and further induces M2‑type macrophages via SLC5A3 to promote HCC tumor growth. The present study identified a novel molecular mechanism by which FBXO22 promotes HCC progression.

Following the publication of the above article, a concerned reader drew to the Editor's attention that, in Fig. 1D, the 'SW1990' and 'Bxpc‑3' data panels were overlapping, suggesting that these data were derived from the same original source where experiments showing different experimental conditions were intended to have been portrayed. In addition, further pairings of overlapping data panels were identified with the Ki67 assay data shown in Figs. 7E and the immunohistochemical data shown in Fig. 10C, suggesting that these figures had similarly been assembled incorrectly. Furthermore, four of the centrally placed flow cytometric plots featured in Fig. 5A appeared to be too similar in terms of the distribution of the data to be confident that these were all derived from independently performed experiments, and finally, some of the western blot data shown in Fig. 4B were strikingly similar to data which had already appeared in another paper, also published in, that featured the same first author (Guanen Qiao). In view of the number of different problems and potential anomalies identified with various of the figures in this paper, the Editor of has decided that this paper should be retracted from the journal on account of an overall lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 44: 593‑607, 2019; DOI: 10.3892/ijmm.2019.4206].

Hepatocellular carcinoma (HCC) treatment remains challenging due to the prevalence of metastasis and chemotherapy resistance. Mitochondrial stomatin‑like protein 2 (STOML2), which is upregulated in various solid tumors, is associated with a poor prognosis; however, its biological function and molecular mechanism in HCC remain unclear. The present study aimed to elucidate the oncogenic mechanism of STOML2 in HCC and to explore its potential as a therapeutic target. Firstly, STOML2 expression in HCC and matched normal liver tissues was analyzed. In addition, STOML2‑knockdown (HCCLM3‑short hairpin RNA‑STOML2) and ‑overexpression (Huh7‑STOML2) cell models were established. Wound healing, Cell Counting Kit‑8 and Transwell assays, and flow cytometry were performed to assess cell proliferation, invasion, migration and apoptosis . Furthermore, the biological function of STOML2 was confirmed in vivo. Co‑immunoprecipitation (co‑IP) and immunofluorescence staining were conducted to validate the interaction of STOML2 with prohibitin (PHB) following the prediction of binding partners. Downstream pathways regulated by STOML2 were identified using western blotting and were further investigated using the RAF1 inhibitor sorafenib. The present study revealed that STOML2 expression was significantly upregulated in HCC tissues and metastatic lesions, and was associated with poor patient prognosis. The experiments showed that STOML2 overexpression promoted proliferation, invasion, migration and autophagy, while inhibiting apoptosis in Huh7 cells. Conversely, STOML2 knockdown reversed these phenotypic changes. Furthermore, co‑IP confirmed the direct interaction between STOML2 and PHB, which activated the RAF/MEK/ERK signaling pathway. The experiments further confirmed that STOML2 overexpression significantly accelerated tumor growth, whereas STOML2 or PHB knockdown inhibited tumor progression. In addition, sorafenib treatment suppressed STOML2‑mediated cell migration and the expression of autophagy‑related proteins by blocking the MAPK pathway. These findings elucidated the molecular mechanism by which STOML2 promotes the malignant progression of HCC and demonstrated that targeted inhibition of the PHB‑MAPK pathway may reverse the pro‑tumorigenic effects of STOML2. STOML2 may serve as both a prognostic biomarker and a therapeutic target in HCC. The current study provides a theoretical foundation for individualized treatment in patients with HCC and high STOML2 expression.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that most of the flow cytometric data shown in Fig. 5A on p. 1020 were strikingly similar to data which had been already been submitted for publication to several other journals that were written by different authors at different research institutes. Owing to the fact that the contentious data in the above article were found to be strikingly similar to data that had already been submitted, or accepted, for publication elsewhere, the Editor of has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 46: 1013‑1028, 2020; DOI: 10.3892/ijmm.2020.4649].

Intrauterine growth restriction (IUGR) is a leading cause of perinatal morbidity and mortality. Oxidative stress is a key factor in the pathogenesis of IUGR. The transcription factor nuclear factor erythroid 2‑related factor 2 (Nrf2) is a key regulator of the cellular antioxidant response. MOTS‑c, a 16‑amino acid peptide derived from the mitochondria, regulates oxidative stress related pathways. However, the effects of MOTS‑c on IUGR remain unclear. The present study aimed to investigate the role of MOTS‑c in hypoxia‑induced placental restriction and IUGR and its underlying mechanisms. Wild‑type and Nrf2 knockout (KO) maternal mice were exposed to hypoxia from gestational days 11 to 17.5 to establish the IUGR model. Human umbilical vein endothelial cells (HUVECs) were used for assays. Maternal serum and placenta MOTS‑c concentration were measured using an enzyme‑linked immunosorbent assay. Hematoxylin and eosin staining, reverse transcription‑quantitative PCR, western blotting, immunohistochemistry and immunofluorescence techniques were employed to evaluate the effects of MOTS‑c treatment on IUGR. It was found that reduced placental content of MOTS‑c was positively correlated with low fetal weight in mice with hypoxia‑induced IUGR. The administration of MOTS‑c (5 mg/kg) significantly attenuated hypoxia‑induced IUGR by promoting placental angiogenesis and inhibiting oxidative stress‑mediated placental dysfunction. Furthermore, these protective effects exerted by MOTS‑c were dependent on Nrf2 activation, as administration of MOTS‑c had no protective role in Nrf2 KO mice or HUVECs pre‑treated with ML385, a Nrf2 inhibitor. Taken together, the present study demonstrated that MOTS‑c mitigated placental injury in hypoxia‑induced IUGR by activation of the Nrf2 signaling pathway, thus potentially identifying a novel therapeutic strategy for hypoxia‑induced IUGR.

During antiviral immunity, MHC‑I molecules display endogenous peptides to CD8 T‑cell receptors, prompting cytotoxic elimination of infected cells. The present study focused on dominant epitopes derived from the nucleocapsid protein (NP) of Hantaan virus (HTNV) and revealed their high affinity for the HLA‑I and H‑2 superfamilies. Through immunogenicity and conservation analyses, four selective epitopes were precisely identified. Molecular docking validated the binding characteristics of selective epitopes with MHC‑I molecules. Bidirectional hierarchical clustering analysis uncovered complex interaction patterns between NP 9‑mer peptides and MHC‑I haplotypes. Moreover, in‑depth investigation of 11 HTNV variants revealed three amino acid substitutions (I241S, E242A and F384I) within the four selective epitopes; however, these substitutions did not significantly affect the pan‑HLA‑I immunoreactivity of these epitopes. Safety assessments highlighted the potential of four selective epitopes for practical applications. Utilizing ELISpot, ELISA and flow cytometry, the immunogenicity of these selective epitopes was comprehensively confirmed. In summary, the present study thoroughly evaluated the pan‑MHC‑I immunoreactivity of HTNV NP, providing a robust foundation for developing effective epitope vaccines for population immunity.

The regulation of methylation and non‑coding RNAs plays important roles in the pathogenesis of osteoporosis. Most microRNAs (miRNAs or miRs) exert their biological functions through target genes. Long non‑coding RNAs function as competing endogenous RNAs. hFOB 1.19 cells were transfected with miR‑4765, LINC00312 and METTL3‑related molecules. LINC00312 and miR‑4765 expression was detected by PCR, whereas cleaved caspase 3 and FOXK2/SFRP1 levels were detected by western blotting. Micro‑computed tomography was used to detect the bone microstructure. Diabetic mice received treatments targeting METTL3 and LINC00312. FOXK2/SFRP1 expression was detected using PCR and immunohistochemistry. The results showed that miR‑4765 overexpression reduced FOXK2/SFRP1 and cleaved caspase 3 expression, causing cell apoptosis. LINC00312 inhibition was observed both and . LINC00312 binds directly to miR‑4765, whereas miR‑4765 binds directly to FOXK2/SFRP1. METTL3 and YTHDF2 directly bind LINC00312 and reduce its expression by altering its methylation levels. In conclusion, LINC00312 promotes the apoptosis of hFOB 1.19 cells by targeting the miR‑4765/FOXK2/SFRP1 axis, and METTL3 regulates LINC00312 expression in a YTHDF2‑dependent manner.

Diabetic nephropathy (DN) and diabetic osteoporosis (DOP) are frequent and debilitating complications of diabetes mellitus (DM), sharing pathological features such as oxidative stress, inflammation and metabolic dysregulation. However, current therapies rarely address these comorbidities simultaneously. In the present study, a type 2 DM rat model presenting both DN and DOP characteristics was established. Rats were treated with Akebia saponin D (ASD), Semaglutide, or their combination. Renal function, calcium‑phosphate metabolism, bone microarchitecture and mechanical properties were evaluated. Network pharmacology, molecular docking and knockdown validation were employed to elucidate underlying mechanisms. Combination therapy markedly improved glomerular structure, decreased fibrosis, restored trabecular bone volume and strength and corrected metabolic imbalance more effectively than monotherapy. Bioinformatic analysis identified the Klotho‑p53 signaling axis as a potential target. ASD exhibited high binding affinity to Klotho in silico and adeno‑associated virus‑mediated Klotho knockdown reversed therapeutic benefits, confirming its pivotal role. ASD and Semaglutide synergistically alleviated both DN and DOP by modulating the Klotho‑p53 axis, offering a promising strategy for comprehensive DM complication management.

Structural birth defects (SBDs) represent a major subset of congenital malformations arising from abnormalities during organogenesis and subsequent tissue morphogenesis. The triad of congenital heart defects (CHDs), orofacial clefts (OFCs) and neural tube defects (NTDs) dominates the global epidemiology of SBDs, collectively contributing to considerable neonatal mortality while imposing profound clinical and socioeconomic burdens. Conventional genetic screening approaches, such as karyotype and non‑invasive prenatal testing, remain limited in their capacity to decipher the complex genomic factors underlying these SBDs. The advent of advanced genomic technologies (including chromosomal microarray analysis and next‑generation sequencing) and integrated genomic analysis methods [such as copy number variation analysis, single nucleotide variation/insertion and deletion analysis and genome‑wide association studies (GWAS)] has enhanced the capacity to identify pathogenic genetic factors, thereby transforming the mode of prenatal diagnosis and genetic counseling. The application of these technologies, by virtue of more accurate diagnosis and finer disease classification, not only provides a more comprehensive basis for assessing disease severity and prognosis in clinical decision‑making but also offers support for implementing targeted intervention and treatment. The present review systematically evaluates state‑of‑the‑art genomic methodologies and computational approaches for detecting genomic aberrations in CHDs, OFCs and NTDs, and integrates insights from GWAS to elucidate the underlying genetic architecture, contributing to achieving precise predictive modeling and targeted therapeutic innovation for SBDs.

Persistent infection with human papillomavirus (HPV) can lead to refractory disease. The HPV E7 protein causes persistent viral infection by disrupting the immune balance of keratinocytes; however, its key mechanism is not yet clear. Overexpression of the HPV E7 gene in normal human epidermal keratinocytes can promote mitophagy in the host cells and inhibit the expression of type I interferon (IFN), as previously confirmed by electron microscopy, immunofluorescence and western blot analysis. In the present study, Siha cells with stable knockdown of HPV16 E7 were constructed, and RNA sequencing at the transcription level and isobaric tags for relative and absolute quantitation analysis at the protein level were performed, with the aim of identifying genes related to mitophagy among the differentially expressed genes. Using immunohistochemistry, PCR and western blotting, significant differences were detected in the expression levels of high‑temperature requirement A serine peptidase 1 (HTRA1) between the knockdown and control groups. The results confirmed that HPV E7 could promote the expression of HTRA1. Furthermore, it was demonstrated that the HPV E7 protein interacted with HTRA1 intracellularly to activate the PTEN‑induced kinase 1 (PINK1)/Parkin pathway in keratinocytes, leading to enhanced mitophagy and reduced expression of type I IFN in host cells. In conclusion, HPV E7 could promote the expression of the HTRA1 gene in keratinocytes, thereby activating mitophagy mediated by the PINK1/Parkin pathway. Furthermore, HPV E7 could inhibit the secretion of type I IFN from cells, thus leading to persistent viral infection. These findings provide novel insights into the association between HPV infection and mitophagy, and may elucidate the mechanisms underlying persistent HPV infection.1.

Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide and their pathological mechanisms have remained a major focus of research. Notably, copper has an essential role in maintaining cardiovascular homeostasis and disruption of copper metabolism can lead to a range of pathological consequences. The present review summarizes the dynamic balance of copper metabolism, clarifies its regulatory network encompassing intestinal absorption, intracellular transport, tissue storage and excretion, and emphasizes the molecular associations between copper dyshomeostasis and CVDs, including atherosclerosis and stroke. Notably, cuproptosis, a newly identified mode of regulated cell death, provides novel insights into the role of copper‑induced cell death in the cardiovascular system. Based on current research progress, the current review also discusses the value of therapeutics that target copper metabolism, such as copper chelators, ionophores and dietary interventions. Furthermore, key unanswered questions are identified, particularly those regarding the specific molecular pathways linking copper homeostasis to cardiovascular function.

Following the publication of this paper, it was drawn to the Editor's attention by an interested reader that, for the western blot experiments shown in Fig. 7A on p. 405, the Bcl‑2 and PCNA blots for the SO‑Rb50 cell line appeared to be identical, albeit it with possibly slightly different exposure time of the gel and different vertical dimensions. Similarly, the BAX and PCNA blots for the Y79 cell line also appeared to be identical, although the blots were rotated by 180° relative to each other, again with possibly slightly different exposure time of the gel and different vertical dimensions. In addition, for the experiments showing transfection efficiency in Fig. 1 on p. 402, the 'SO‑Rb50/x100/PAX6‑RNAi GFP' and 'Y79/x200/Ctrl GFP' data panels contained overlapping data, and the 'SO‑Rb50/x200/PAX6‑RNAi GFP' and 'Y79/x100/Ctrl GFP' data panels similarly contained overlapping data, suggesting that these pairings of panels had been placed in this figure the wrong way around. Upon contacting the authors about these issues, they realized that Figs. 1 and 7 in this paper had inadvertently been assembled incorrectly. The revised versions of Fig. 1, now featuring the correct data for the PCNA blots for both the SO‑Rb50 and the Y79 cell lines, and Fig. 7, now showing the correctly positioned data panels for the 'SO‑Rb50/x100/PAX6‑RNAi GFP' and 'Y79/x200/Ctrl GFP' experiments, are presented on the next page. The authors wish to emphasize that the errors made in assembling the data in these Figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused. [International Journal of Molecular Medicine 34:  399‑408, 2014; DOI: 10.3892/ijmm.2014.1812].

Following the publication of this paper, a concerned reader drew to the Editor's attention that, regarding the western blots shown in Fig. 1A, where the expression levels of salt‑inducible kinase 1 were detected in ovarian cancer tissues, the β‑actin loading controls for patients 4, 6 and 7 were strikingly similar in appearance [also note that, in view of having not received a timely response to this query from the authors, an Expression of concern (DOI: 10.3892/ijmm.2025.5627) was published for this paper]. Moreover, several of the protein bands in this figure were strikingly similar to data which subsequently appeared in another paper written by different authors at different research institutes that was also published in the journal , although this paper has since been retracted. The authors have subsequently replied to say that they are unable to retrieve a portion of the original experimental data, and therefore wish to retract this paper. All the authors agree with the retraction of this article. Both the authors and the Editor of apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 37: 1601‑1610, 2016; DOI: 10.3892/ijmm.2016.2553].

Temporomandibular joint (TMJ) synovitis is a chronic inflammatory condition prevalent in temporoman-dibular disorders, characterized by synovial inflammation and bone degradation. Quercetin, a natural flavonoid with diverse bioactive properties, is investigated for its potential in ameliorating TMJ synovitis by targeting the p38 MAPK pathway. Using network pharmacology and and models, the effects of quercetin on synoviocytes and inflammatory responses were evaluated. Results showed quercetin's significant inhibition of synoviocyte proliferation, promotion of apoptosis and reduction of inflammatory cytokines. Moreover, quercetin demonstrated stability in binding to critical targets like MAPK14 and led to downregulation of phosphorylated p38 MAPK and JNK. , quercetin improved synovial tissue architecture and mitigated bone destruction. Mechanistic studies confirmed the dependency of effects of quercetin on the p38 MAPK pathway, supported by functional experiments using pathway agonists and inhibitors. The present study underscored the potential of quercetin in treating TMJ synovitis by modulating inflammatory signaling, promoting cell apoptosis and preserving bone integrity, thereby offering novel insights into therapeutic strategies for TMJ‑related synovitis.

Protein homeostasis, or proteostasis, refers to the integrated quality control systems that regulate protein synthesis, folding, post‑translational modification, trafficking and degradation to maintain proteome stability and function. Disruption of these processes, including abnormal synthesis, misfolding or impaired degradation, results in proteostasis collapse and underlies the pathogenesis of cancer, neurodegeneration, cardiovascular disease and metabolic syndromes. Recent studies have highlighted FK506‑binding proteins (FKBPs), a family of immunophilins defined by a conserved peptidyl‑prolyl cis‑trans isomerase domain, as pivotal modulators of proteostasis. By modulating protein folding, stabilizing complexes, regulating endoplasmic reticulum stress and directing selective degradation, FKBPs establish direct links between proteostasis regulation and disease progression. This review presents the first comprehensive synthesis of FKBP‑mediated control of proteostasis across diverse clinical contexts. It analyzed how their structural features confer regulatory potential and elucidate their roles in proteome remodeling in cancer, pathogenic protein aggregation in neurodegenerative disorders, ion channel stabilization in cardiovascular dysfunction and kinase phosphorylation in metabolic regulation. By integrating these diverse actions within a unified proteostasis framework, FKBPs are proposed as versatile regulators and promising therapeutic targets, providing new perspectives on the proteostasis‑disease axis and opportunities for precision intervention across multiple organ systems.