Exercise-driven cellular autophagy: A bridge to systematic wellness

Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Exercise enhances health by supporting homeostasis, bolstering defenses, and aiding disease recovery. It activates autophagy, a conserved cellular process essential for maintaining balance, while dysregulated autophagy contributes to progression. Despite extensive research on exercise independently, their interplay remains insufficiently understood. This review explores the molecular mechanisms of exercise-induced in various tissues, focusing key transduction pathways. examines how different types trigger specific autophagic responses, balance addressing systemic dysfunctions. The also highlights signaling pathways involved, roles protecting organ function, reducing risk, promoting longevity, offering clear understanding link between autophagy. Exercise-induced is governed highly coordinated dynamic integrating direct indirect mechanical forces biochemical signals, linking physical activity across multiple systems. Its activation influenced modality, intensity, duration, individual biological characteristics, including age, sex, muscle fiber composition. Aerobic exercises primarily engage AMPK mTOR pathways, mitochondrial quality homeostasis. Anaerobic training PI3K/Akt signaling, modulating molecules like FOXO3a Beclin1 drive repair. In pathological contexts, proteostasis, tissue regeneration, benefiting conditions sarcopenia, neurodegeneration, myocardial ischemia, metabolic disorders, cancer. However, excessive may lead overactivation, leading atrophy or cardiac remodeling. underscores critical need balanced regimens maximize therapeutic efficacy minimizing risks. Future should prioritize identifying reliable biomarkers, optimizing protocols, with pharmacological strategies enhance outcomes.

Language: Английский

---

Mammalian nucleophagy: process and function

Autophagy, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 19, 2025

The nucleus is a highly specialized organelle that houses the cell's genetic material and regulates key cellular activities, including growth, metabolism, protein synthesis, cell division. Its structure function are tightly regulated by multiple mechanisms to ensure integrity genomic stability. Increasing evidence suggests nucleophagy, selective form of autophagy targets nuclear components, plays critical role in preserving clearing dysfunctional materials such as proteins (lamins, SIRT1, histones), DNA-protein crosslinks, micronuclei, chromatin fragments. Impaired nucleophagy has been implicated aging various pathological conditions, cancer, neurodegeneration, autoimmune disorders, neurological injury. In this review, we focus on mammalian cells, discussing its mechanisms, regulation, cargo selection, well evaluating therapeutic potential promoting human health mitigating disease.

Language: Английский

---

Genetic and pharmacological correction of impaired mitophagy in retinal ganglion cells rescues glaucomatous neurodegeneration

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 15, 2025

Progressive loss of retinal ganglion cells (RGCs) and degeneration optic nerve axons are the pathological hallmarks glaucoma. Ocular hypertension (OHT) mitochondrial dysfunction linked to neurodegeneration vision in However, exact mechanism leading glaucomatous is poorly understood. Using multiple mouse models OHT human eyes from normal glaucoma donors, we show that induces impaired mitophagy RGCs, resulting accumulation dysfunctional mitochondria contributing neurodegeneration. reporter mice, precedes Notably, pharmacological rescue via Torin-2 or genetic upregulation RGC-specific Parkin expression restores structural functional integrity RGCs their ex-vivo retinal-explant cultures. Our study indicates contributes oxidative stress, Enhancing represents a promising therapeutic strategy prevent

Language: Английский

---

Roles of Oxidative Stress and Autophagy in Alcohol-Mediated Brain Damage

Antioxidants, Journal Year: 2025, Volume and Issue: 14(3), P. 302 - 302

Published: Feb. 28, 2025

Excessive alcohol consumption significantly impacts human health, particularly the brain, due to its susceptibility oxidative stress, which contributes neurodegenerative conditions. Alcohol metabolism in brain occurs primarily via catalase, followed by CYP2E1 pathways. Excess metabolized generates reactive oxygen/nitrogen species (ROS/RNS), leading cell injury altering many different Elevated stress impairs autophagic processes, increasing post-translational modifications and further exacerbating mitochondrial dysfunction ER death. The literature highlights that alcohol-induced disrupts autophagy mitophagy, contributing neuronal damage. Key mechanisms include dysfunction, epigenetics, accumulation of oxidatively modified proteins, lead neuroinflammation impaired cellular quality control. These processes are exacerbated chronic exposure, resulting suppression protective pathways like NRF2-mediated antioxidant responses increased changes brain. Alcohol-mediated neurotoxicity involves complex interactions between metabolism, regulation, influenced various factors such as drinking patterns, nutritional status, genetic/environmental factors, highlighting need for molecular studies unravel these develop targeted interventions.

Language: Английский

---

Autophagy-dependent versus autophagy-independent ferroptosis

Trends in Cell Biology, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Ferroptosis is an iron-dependent cell death pathway that, until recently, has been considered to be dependent on autophagy. However, recent studies have reported conflicting results, raising the question about which contexts determine roles of autophagy in ferroptosis. This opinion article addresses this by summarizing and/or diseases a driver or suppressor The execution ferroptosis depends levels (labile) iron, unsaturated (phospho)lipids and free radicals. We propose that context these three factors their upstream pathways are differentially regulated dictates whether positively negatively regulates

Language: Английский

---

The Women In Autophagy network empowers global equity in science

Nature Aging, Journal Year: 2025, Volume and Issue: unknown

Published: March 12, 2025

Language: Английский

---

How does autophagy impact neurological function?

The Neuroscientist, Journal Year: 2025, Volume and Issue: unknown

Published: March 13, 2025

Autophagies describe a set of processes in which cells degrade their cytoplasmic contents via various routes that terminate with the lysosome. In macroautophagy (the focus this review, henceforth autophagy), contents, including misfolded proteins, protein complexes, dysfunctional organelles, and pathogens, are captured within double membranes called autophagosomes, ultimately fuse lysosomes, after degraded. Autophagy is important maintaining neuronal glial function; consequently, disrupted autophagy associated neurologic diseases. This review provides broad perspective on roles CNS, highlighting recent literature furthers our understanding multifaceted role healthy nervous system.

Language: Английский

---

Transcription factor EP300 targets SIRT5 to promote autophagy of nucleus pulposus cells and attenuate intervertebral disc degeneration

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2025, Volume and Issue: unknown, P. 119933 - 119933

Published: March 1, 2025

Language: Английский

---

Fucoidan for potentially treating amblyopia: Autophagy-associated targets and therapeutic mechanisms

Carbohydrate Polymer Technologies and Applications, Journal Year: 2025, Volume and Issue: unknown, P. 100770 - 100770

Published: March 1, 2025

Language: Английский

---

The inducible role of autophagy in cell death: emerging evidence and future perspectives

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 26, 2025

Autophagy is a lysosome-dependent degradation pathway for recycling intracellular materials and removing damaged organelles, it usually considered prosurvival process in response to stress stimuli. However, increasing evidence suggests that autophagy can also drive cell death context-dependent manner. The bulk of contents the accumulation autophagosomes are recognized as mechanisms induced by alone. other forms regulated (RCD) whose not related excessive autophagic vacuolization. Notably, few reviews address studies on transformation from RCD, underlying molecular still vague. This review aims summarize existing autophagy-mediated elucidate mechanism which initiates comprehensively understand role determining fate. highlights prodeath effect autophagy, distinct generally perceived cytoprotective role, its mainly associated with selective proteins or organelles essential survival direct involvement machinery death. Additionally, this need better manipulation activation inhibition different pathological contexts, depending clinical purpose.

Language: Английский

---