Doxorubicin (DOX) induces dose-dependent cardiotoxicity, primarily through oxidative stress and metabolic dysregulation. Although NAD deficiency has been implicated in cardiovascular pathology, its role in DOX-induced cardiotoxicity (DIC) remains poorly understood. This study investigated NAD metabolism dysregulation as a redox-sensitive mechanism in DIC pathogenesis.

Epilepsy is a chronic neurological condition characterized by recurrent seizures, often linked to neuroinflammation and oxidative stress that exacerbate neuronal injury. Neuropilin-2 (NRP2) and Nuclear Factor-Kappa B (NF-κB) are key mediators in these pathways. This study evaluated the neuroprotective effects of emodin, a bioactive anthraquinone with antioxidant and anti-inflammatory properties, in a pentylenetetrazole (PTZ)-induced mouse model of epilepsy.

Reactive nitrogen species (RNS) play a pivotal role in tumorigenesis through complex regulatory networks within the tumor microenvironment (TME). This review summarizes recent advances in understanding RNS-mediated mechanisms, focusing on core components and their concentration-dependent bidirectional effects on tumor cell proliferation, apoptosis, invasion, and metabolism. It explores RNS sources in the TME, including autonomous synthesis by tumor cells and secretion by immune cells (e.g., TAMs, TANs), and their modulation of key signaling pathways (e.g., PI3 K/Akt, NF-κB, HIF-1α). Additionally, the review discusses RNS-mediated regulation of immune responses and angiogenesis, highlighting their dual roles in promoting tumor progression and enabling immune evasion. Finally, it outlines potential clinical applications, such as RNS-targeted diagnostic probes and therapeutic strategies (e.g., iNOS inhibitors, NO donors), providing a foundation for precision oncology.

Smoking is a major etiological factor in numerous chronic lung diseases. However, the precise underlying mechanisms remain incompletely elucidated. In this study, we investigated the effects of cigarette smoke extract (CSE) on mitochondrial oxidative phosphorylation (OXPHOS), mitochondrial structure, and the antioxidant regulator Nuclear factor erythroid 2-related factor 2 (NRF2) in a rat lung epithelial-T-antigen negative cell line (RLE-6TN), focusing on the associated molecular pathways. CSE exposure significantly reduced cell viability, induced oxidative-antioxidant imbalance, and disrupted OXPHOS complex subunit expression and mitochondrial ultrastructure. Furthermore, an increased BCL2-Associated X (BAX) / B-cell lymphoma/leukemia 2 (BCL2) ratio activated the intrinsic apoptosis pathway. NRF2 knockdown exacerbated CSE-induced mitochondrial damage and apoptosis. Co-immunoprecipitation (co-IP) analysis revealed a direct interaction between NRF2 and Fatty Acid Synthase (FASN). CSE treatment significantly reduced NRF2-FASN binding. Notably, FASN knockout amplified oxidative stress, exacerbated damage to OXPHOS and mitochondrial structure, and diminished NRF2 expression and nuclear translocation. Collectively, our findings demonstrate that CSE exposure impairs NRF2 expression and nuclear translocation by disrupting FASN expression and its interaction with FASN. This impairment leads to mitochondrial OXPHOS dysfunction, structural damage, and ultimately apoptosis. Our findings identify FASN as a potential therapeutic target for mitigating smoking-associated lung injury.

Long non-coding RNAs (lncRNAs) are increasingly recognized in keloid pathogenesis. This study investigates the role and mechanisms of HOXA11-AS in keloid formation.

Oxidative stress plays a critical role in the degeneration of midbrain dopaminergic (DA) neurons in Parkinson's disease (PD). However, therapies targeting redox mechanisms are hindered by a lack of scalable and inexpensive redox-focused preclinical models.

Spinal cord injury (SCI)-induced mitochondrial dysfunction in microglia exacerbates neuroinflammation and neurological deficits. Monoammonium glycyrrhizinate (MAG), a bioactive liquorice-derived compound, exhibits anti-inflammatory and antioxidant properties; however, its effects on microglial mitochondria remain unknown.

Sensory neurons relay the pain signals to the brain via the nociceptive system. Notably, reactive oxygen species (ROS) serve as signaling molecules in the somatosensory system; however, their contribution to sensing noxious stimuli remains poorly understood.

Diabetic nephropathy (DN) is the most common complication of diabetes mellitus. It has shown that the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) could attenuate DN. To identifiy novel Nrf2 activators targeting DN, we explored drynachromoside A (DCSA) from and .

Acetaminophen (APAP) overdose is the leading cause of drug-induced acute liver failure. Sesamin (Ses), a natural polyphenolic compound, possesses diverse pharmacological properties. This study was to explore the effects of Ses on APAP-induced liver injury and the underlying molecular mechanism.

Mitochondrial dynamics are tightly coupled with cellular redox homeostasis; however, the underlying regulatory mechanisms remain poorly defined.

Lung cancer is one of the leading causes of cancer-related deaths worldwide with limited treatment options available. The anti-tumor effects of the TrxR inhibitor Butaselen (BS/BS1801) on lung cancer and its underlying mechanisms remain unknown.

Tropoelastin (TE), the soluble precursor of elastin, is critical for the elasticity of arteries, lungs, and skin. Oxidative damage to TE has been implicated in vascular diseases, but the isoform-specific effects remain poorly understood. Hypochlorous acid (HOCl), generated by the enzyme myeloperoxidase (MPO) targets extracellular matrix proteins during inflammatory processes. However, the differential susceptibility and functional consequences in specific TE isoforms are unknown.

The adaptation of the redox system and bioenergetics is a major factor contributing to cancer metabolism. Redox therapy is promising but still requires molecular studies that consider the reactive species interactome (RSI) concept, which integrates reactive oxygen, nitrogen, sulfur, carbonyl species, and redox enzymes. Our aim was to decipher the role of the RSI in glioblastoma (GBM), including by challenging the RSI with the MnTBAP redox agent.

Melatonin is a powerful free radical scavenger, with cardioprotective effects; however, the mechanism of this cardioprotective activity remains unclear. We hypothesized that melatonin inhibits ferroptosis and protects cardiomyocytes through suppression of the ataxia telangiectasia mutated (ATM)/p53 signaling pathway and reduction of lipid peroxidation.

This review aims to explore the roles and mechanisms of cytochrome P450 subfamily 1 (CYP1) enzymes in acute lung injury (ALI), and to discuss their potential as therapeutic targets.

Reactive oxygen species (ROS) are short-lived and act in a site-specific manner, underscoring the importance of identifying the subcellular localization of their sources. ROS-generating NADPH oxidases (NOX) regulate pancreatic beta cell (dys)function. However, their subcellular localization and cytokine-mediated regulation in these cells remain largely unknown. We characterized the expression, subcellular localization and time-dependent cytokine-induced regulation of NOX isoforms in beta cells.

Iron continues to be linked to the pathogenesis of neurodegenerative disorders including HIV-1 associated neurocognitive disorders (HAND). People with HIV-1 who use opioids have a higher risk of developing HAND, and HIV-1 proteins and opioids disrupt endolysosome iron homeostasis, increase reactive oxygen species (ROS), and cause neural cell death. Endolysosomes are subcellular acidic organelles that regulate iron metabolism and redox homeostasis. HIV-1 gp120 and opioids induce endolysosome iron release, increasing cytosolic and in mitochondrial iron and ROS and inducing neurotoxicity. However, ROS represent only part of the reactive species interactome (RSI) and little is known about the extent to which HIV-1 proteins and opioids affect the RSI.

Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), remains a major global health threat due to prolonged treatment and drug-resistant strains. Host-directed therapy (HDT), which modulates host-pathogen interactions, offers potential to shorten treatment and limit resistance. This study investigates the effects of Scutellarin (SCU), a flavonoid from Scutellaria baicalensis, on Mtb-infected macrophages within the HDT framework.

Sepsis-induced cardiomyopathy (SIC) involves ferroptosis, an iron-dependent cell death. Hypoxia-inducible factor-1α (HIF-1α) regulates autophagy and apoptosis, but its role in ferroptosis remains unclear. This study investigates the interaction between the HIF1A/BNIP3 signaling pathway and the ferroptosis axis, SLC7A11/GPX4, in septic myocardial injury.

Current treatment options for head and neck squamous cell carcinoma (HNSCC) are limited. Aspartate aminotransaminase (GOT1) plays an important role in cancer development but its role in HNSCC remains unknown. We combined proteomics and metabolomics to identify high GOT1expression in human cancer tissues. The effects of GOT1 knockdown on cancer cell proliferation were confirmed using CCK8, wound healing assays, colony formation assays, and EdU assays. The anti-apoptotic ability of cancer cells was evaluated using TUNEL assay and flow cytometry. GOT1 knockdown caused mitochondrial dysfunction and was characterized by reduced mitochondrial membrane potential and altered expression of mitochondrial electron transport chain complexes and key transcription factors, as measured by JC-1 and qRT-PCR. Given that mitochondria are the primary source of reactive oxygen species (ROS), we assessed cellular ROS and mitochondrial superoxide levels by flow cytometry and found a significant increase. GOT1 knockdown increased the sensitivity of cells to cisplatin and decreased the volume of tumors in vivo. In summary, GOT1 knockdown inhibited proliferation and promoted apoptosis via ROS overproduction from mitochondrial dysfunction, thereby increasing cisplatin sensitivity. RNA-seq further identified aldehyde dehydrogenase 3A1 (ALDH3A1) as potentially downstream target of GOT1. These findings suggest that GOT1 knockdown may improve clinical outcomes in HNSCC.