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In this study, researchers found that mitochondrial complex I plays a crucial role in regulating innate immunity and bone remodeling, with Ndufs4 deletion causing systemic inflammation and osteopetrosis through various metabolic shifts and cellular mechanisms.

This study found that inhibiting autophagy in mouse preputial glands alters lipid metabolism, delays aging-related duct changes, and reduces pheromone production, indicating autophagy's critical role in gland homeostasis and cell breakdown during secretion.

In this study published in Nature, researchers explored how hair follicle stem cells manage apoptotic cell clearance while maintaining their regenerative roles, identifying significant molecules involved in sensing and engulfing dying cells to sustain tissue health.

This study found that downregulating PI3K in common bean severely impaired symbiosis with beneficial microorganisms, indicating an essential role for autophagy-related processes in these mutualistic interactions.

This study found that blocking autophagy in Atg7-deficient mouse hair keratinocytes altered the molecular composition of hair shafts by increasing the abundance of proteins involved in protein turnover while keratins remained unchanged, highlighting autophagy's role in reducing non-cytoskeletal protein concentrations in hair.

This review explores the complex relationships between ferroptosis, anastasis, and chemoresistance in cancer therapy, highlighting the potential of combining ferroptosis with immunotherapy to overcome resistance and improve personalized cancer treatments.

This pilot study suggests that autophagy is crucial for anagen maintenance in human hair follicles, and targeting this process may help manage hair growth disorders.

In this study, researchers found that autophagy is crucial for maintaining the mature protein composition of hair shafts, with its disruption leading to increased levels of various proteins, suggesting potential diagnostic applications for detecting impaired autophagy through hair proteomic analysis.

This review examines the development and challenges of using PROTACs, a targeted protein degradation strategy, to treat cancer by degrading specific proteins like PARPs and GPX4, highlighting issues such as target diversification and bioavailability.

In this study, researchers developed de novo designed hetero-bifunctional proteins as an alternative approach for targeted protein degradation, successfully targeting BCL-xL for degradation in cells and inducing apoptosis, which may expand the range of addressable E3 ligases and disease targets.

In this study, researchers engineered extracellular vesicles enriched with functional mitochondria to enhance healing in diabetic wounds by reversing mitochondrial and immunometabolic dysfunction in macrophages.

In this study, DMC selectively eliminated senescent cells in old mice, prevented hair loss, improved motor coordination, and reduced senescence-associated secretory factors, suggesting its potential as a senolytic treatment.

This study found that sustained intracellular acidosis in mice was associated with shortened lifespan, early aging signs, and impaired autophagy.

This review highlights the potential of PROTAC technology in drug discovery for previously undruggable targets, particularly in cancer therapy, while emphasizing the urgent need to discover more E3 ligase recruiters to optimize targeted protein degradation.

This study identified seven genes that may serve as biomarkers for diagnosing skin cutaneous melanoma by analyzing the relationship between UV exposure, ferroptosis, and the cancer's pathology.

In this study, researchers found that keratinocyte-specific deletion of the autophagy mediator Atg16l1 in mice heightened skin inflammation and cancer responses, altered hair follicle stem cell activity, and sensitized keratinocytes to cell death.

This review discusses the regulation of the MiT-TFE family transcription factors, particularly TFEB, through phosphorylation-mediated subcellular localization and reports no new clinical results.

In this study, researchers found that human adipose tissue-derived mesenchymal stromal cells exhibit significant phagocytic ability against various particles and pathogens, which might enhance strategies for addressing specific local and systemic infections due to their regenerative properties.

This study suggests that inhibiting PKC, similar to rapamycin treatment, can extend lifespan and reduce neurological symptoms and inflammation in mice with mitochondrial dysfunction, potentially involving the mTORC2 pathway.

This study found that autophagy-related gene expressions in bleomycin-induced mouse skin fibrosis initially increased and then decreased, implying autophagy activation may potentially reverse skin fibrosis.

This study demonstrated that de novo designed bifunctional proteins can target and degrade BCL-xL, leading to cell apoptosis, suggesting a new approach to targeted protein degradation therapy.

This study found that removing autophagy in keratinocytes led to increased skin inflammation, higher risk of skin tumors, and early hair follicle activation in mice.

Martin-Perez et al. show that rapamycin's beneficial effects in a mouse model of Leigh syndrome are linked to the downregulation of protein kinase C.

This study suggests that specific mutations in the MFN2 gene, including the p.Arg707Trp allele, can result in tissue-selective mitochondrial dysfunction leading to excessive upper body fat growth and low leptin levels.

This study found that in mouse embryonic fibroblast cells lacking autophagy function, overexpression of Atg5 increased cell proliferation, while restoring autophagy reversed this effect, highlighting Atg5's dual role in tumorigenesis depending on autophagy conditions.

In this study on mouse preputial glands, suppressing ATG7-dependent autophagy delayed age-related changes, affected lipid metabolism, and reduced pheromone production, highlighting autophagy's roles in glandular homeostasis and cell breakdown.

This study identified that α-ketobutyrate (α-KB) extends lifespan and improves health markers in Caenorhabditis elegans and aged mice by modulating pyruvate metabolism and activating AMPK pathways, with potential implications for human anti-aging treatments.

This study found that FLCN deficiency in mice muscles led to increased mitochondrial biogenesis and a metabolic shift towards oxidative phosphorylation, with a similar advantage observed in FLCN-null kidney cancer cells.

This review discusses the role of autophagy in skin cells and its potential implications for treating immune-related skin diseases, reporting no new clinical results.

This study suggests that autophagy is essential for regulating TLR3-mediated regenerative processes in human keratinocytes.