Migrasomes are specialized organelle that form during cell migration and play a critical role in intercellular communication and disease progression. First discovered in 2012 and reported in 2015, these organelles are characterized by their unique biogenesis on retraction fibers and their role in spatiotemporal signaling, distribution of bioactive molecules, and maintenance of cellular homeostasis. This review provides a comprehensive overview of migrasome biology, exploring their discovery, mechanisms of formation, physiological functions, and pathological implications. We examine their dual roles in both health and disease, highlighting their potential as diagnostic biomarkers and therapeutic targets. Additionally, we discuss the challenges and future directions in migrasome research, emphasizing the importance of foundational discoveries and advanced methodologies to fully realize their clinical potential.

Skeletal muscle is a highly adaptable tissue that plays a central role in overall health. The dynamic balance between muscle protein synthesis and breakdown governs skeletal muscle mass maintenance. Increased loading and hyperaminoacidemia (via protein ingestion) are positive drivers of skeletal muscle protein accretion, which, when combined, drive a hypertrophic phenotypic adaptation. In contrast, unloading (disuse) results in skeletal muscle atrophy and metabolic dysregulation. Hypertrophy enhances metabolic health and functional capacity, underscoring the importance of understanding the mechanisms that regulate this process. External variables, such as resistance exercise and dietary protein, influence hypertrophy; however, resistance exercise is the primary driver, with protein playing a minor supporting role. Signals from external inputs - loading (resistance exercise) and nutritional manipulation (protein ingestion) - are sensed and transduced into intracellular pathways that promote muscle protein synthesis, yet the precise mechanisms underlying their integration remain incompletely understood. This review summarizes current knowledge on how resistance exercise and dietary protein converge on the intracellular level to regulate skeletal muscle hypertrophy in humans.

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MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level. Several studies have highlighted their role as key regulators of different physiological processes that underly retinal homeostasis. Recent evidence suggests that they play a role not only at the intracellular level but also extracellularly, participating in cell-cell crosstalk by being transported via extracellular vesicles (EVs). Moreover, changes in miRNA expression levels have been associated with different forms of retinal diseases, such as Inherited Retinal Diseases (IRDs). IRDs are a group of genetic disorders characterized by photoreceptor cell death and retinal degeneration. Notably, miRNAs can simultaneously regulate multiple molecular pathways associated with disease initiation and progression. Finally, modulation of miRNAs through upregulation or downregulation has shown beneficial effects in different IRD mouse models. Here, we provide a comprehensive overview of retinal miRNA expression profiles in both healthy and IRD conditions and explore their potential as therapeutic targets for clinical applications.

Advances in wearable sensing technology are driving a new era of personalized health monitoring. In contrast to the hard, rigid form factors of conventional wearable sensors, these emerging skin-interfaced systems support high-quality physiological measurements across biophysical, biochemical, and kinematic signals of interest. These platforms enable continuous monitoring of complex physiological processes with unprecedented detail as a result of a seamless, conformal skin-interface and advanced wireless communications capabilities. These platforms integrate flexible materials, miniaturized electronics, and wireless communication to provide detailed physiological data during daily activities. This review examines how skin-interfaced wearables are advancing patient care, remote monitoring, and large-scale health studies. We highlight critical barriers to clinical adoption including interpreting data, validating devices, and integration into healthcare systems. Key opportunities include sustainable manufacturing, point-of-care fabrication, and development of disease-specific digital biomarkers. By addressing these challenges through collaboration among engineers, clinicians, and data scientists, wearable sensors can expand patient access to advanced physiological monitoring and transform personalized medicine.

The lung, classically viewed as a gas exchange organ, is increasingly recognized as a dynamic sensory interface that continuously monitors the external environment and communicates with the brain to shape physiology and disease. Vagal sensory neurons provide the predominant afferent innervation of the airways, displaying striking molecular diversity, distinct projection patterns, and specialized terminal morphologies that enable detection of mechanical, chemical, and immune-derived signals. These neurons orchestrate critical homeostatic functions, including breathing regulation, airway protection, and cardiopulmonary integration, while also contributing to pathological processes such as airway hyperreactivity, inflammation, and neuroimmune remodeling. Recent advances in molecular profiling, genetic tools, and circuit-mapping approaches have revealed new principles of vagal sensory organization, yet fundamental questions remain about how specific neuronal subtypes encode diverse environmental inputs, how their signals are integrated within central circuits, and how disease reshapes these pathways. This review synthesizes current knowledge of lung-innervating vagal sensory neurons, emphasizing their roles in neuroimmune crosstalk, central integration, and disease pathogenesis. We highlight unresolved controversies and propose future directions aimed at decoding the molecular logic of airway sensation, mapping neuroimmune signaling, and developing organ-specific neuromodulation strategies to treat lung diseases. Together, these insights position vagal sensory pathways as central players in the lung-brain axis and promising therapeutic targets at the intersection of respiratory, immune, and neural health.

In recent years, our understanding of copper metabolism in humans has advanced considerably, driven in large part by insights from genetic disorders. Studies of Menkes disease, Wilson disease, MEDNIK and KIDAR syndromes, and most recently CTR1 deficiency, have illuminated the fundamental principles of copper acquisition, intracellular distribution, and systemic elimination. These discoveries revealed not only the canonical roles of CTR1, ATP7A, and ATP7B, but also uncovered auxiliary pathways of copper uptake, novel chaperone and organelle-specific distribution mechanisms, and the importance of trafficking adaptors in maintaining copper balance. Beyond its classical enzymatic functions, copper has emerged as a dynamic regulator of cell signaling, autophagy, metabolism, and immune surveillance, with mitochondrial dysfunction and cuproptosis representing key pathogenic outcomes of copper imbalance. The expanding view of copper as both a nutrient and a signaling ion highlights the complexity of its physiological regulation. In this review, we summarize the current knowledge of human copper homeostasis, focusing on how lessons from inherited disorders continue to redefine our understanding of copper physiology and inform therapeutic approaches.

Maintenance of body water and sodium homeostasis is essential to terrestrial life, with the kidney classically viewed as the principal regulator. However, this kidney-centric model does not fully account for the various physiological and pathophysiological states, including the paradoxical association between water loss and hypertension. This review proposes a shift in perspective toward "water conservation" as a core concept, highlighting the integrated and reciprocal crosstalk between the kidney and the skin. Evidence from animal models of skin barrier defects and renal injury demonstrates that primary water loss from one organ elicits a compensatory water-conserving response. A key mechanism in this adaptation is vasoconstriction, which reduces water loss across these barriers, and in turn, elevates systemic blood pressure. We further discuss evidence showing that the skin is not merely a passive barrier but also an active hemodynamic organ, with local molecular pathways-such as the hypoxia-inducible factor and renin-angiotensin systems-capable of directly influencing systemic blood pressure. Finally, we address the limitations of the current paradigms by examining tissue-specific sodium storage and the uncoupling of water and sodium balance, underscoring the need for integrated tissue-level analysis. This review provides a conceptual framework that reevaluates the roles of the kidney and skin in regulating body fluids and offers new insights into the physiology of body water and blood pressure regulation.

Under conditions of exercise the heart and lungs are linked in important ways. First, both the heart and lungs are linked in series as pumps for O and CO transport. Second they are mechanically linked owing to their location within the thorax. This means that changes in lung volume (and intrathoracic pressure) will influence cardiac filling and ejection. The respiratory muscles cyclically contract during exercise to allow for gas exchange. This ensures that the partial pressures of O and CO in the blood are largely kept within narrow limits, while the heart and circulatory system ensures gas transport to and from the tissues. The increase in metabolic rate during exercise requires substantial increases in both cardiac output and ventilation, meaning that cardiopulmonary interactions become more pronounced. In this review we explore they physiological interactions between the respiratory system and circulatory systems by asking two inter-related questions. First, what are the mechanical interactions between the respiratory and circulatory systems? Second, what are the respiratory influences on sympathetic vasomotor outflow and blood flow distribution during exercise? We end with a summary of recent studies that have addressed questions of respiratory-circulatory interactions with respect to sex differences and cardiopulmonary disease.

Female reproductive aging is the earliest manifestation of aging in humans, with fertility declining due to reduced oocyte quality well before menopause. Menopause marks the definitive end of reproductive potential and the onset of increased risk for multiple age-related, chronic diseases. Emerging evidence links reproductive disorders, from infertility to widespread gynecological conditions such as polycystic ovarian syndrome, with elevated risks of premature morbidity and mortality. Indeed, it is increasingly evident that even normal reproductive transitions such as puberty, pregnancy, and menopause, act as physiological inflection points that shape long-term systemic health. Yet, fertility continues to be viewed primarily through the prism of procreation, with limited knowledge of the underlying biological mechanisms and scarce clinical focus on its broader health implications. Recent discoveries elucidating the genetic basis of reproductive traits combined with advances in our understanding of fundamental aging mechanisms offer a compelling framework to address these persistent knowledge gaps with far-reaching public-health consequences. This review synthesizes the current knowledge on how reproductive aging, normal reproductive phases and major reproductive dysfunctions influence long-term health trajectories and argues for a shift toward integrated, lifespan-based approaches to reproductive health in research and clinical care.

Oocyte meiosis, the process of egg cell formation, requires a highly regulated cell cycle with many unique features compared to somatic cell division. On the journey to create a healthy embryo, this special cell carries a heavy responsibility and must navigate a remarkable number of complex challenges. Most oocytes will never complete this journey, less than 0.1% are ever ovulated, and fewer are viable. However, the few that do complete, manage by the execution of a series of extraordinary adaptations through two rounds of cell division. In this review we discuss some of these challenges and the adaptations that have evolved to mitigate them. This is not intended to be a comprehensive review of the cell cycle in oocytes meiosis, but to highlight some of the differences between oocyte meiosis and a typical mitosis. We discuss features that make this cell unique and the cell cycle regulatory mechanisms that support them. A salute to the few that make it and those that are sacrificed along the way.

As populations age worldwide, understanding the biology of aging and its contribution to disease becomes increasingly important. Cellular senescence, a hallmark of aging, plays a pivotal role in shaping inter-organ communication and systemic health. Once viewed primarily as a local mechanism to prevent the proliferation of damaged cells, senescence is now recognized as a dynamic, multifaceted process that influences physiology across the lifespan. Through senescence-associated secretory phenotype (SASP) proteins and other signaling modalities, including metabolites, extracellular vesicles, immune cells, and neural circuits, senescent cells contribute to both homeostatic regulation and the propagation of chronic inflammation, fibrosis, and age-related disease. These effects are often context-dependent, and senescence in one organ can influence distant tissues, driving asynchronous aging and disease vulnerability. This review examines the mechanisms by which senescent cells facilitate inter-organ communication, including emerging roles for blood-borne factors, immune cell dynamics, and neuroendocrine signals. We highlight illustrative examples of organ crosstalk and emphasize the potential translational relevance of these pathways. We also examine therapeutic strategies aimed at modulating senescence, including senolytics, senomorphics, and interventions targeting specific SASP components, as well as the potential of lifestyle modifications to mitigate biological aging. Understanding senescence and the associated inter-organ communication offers new insights into aging biology and opens promising avenues for addressing age-related diseases in an integrated, organ-spanning framework.