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This study found that a long-term astrocyte culture model can effectively study astrocyte senescence and suggests minoxidil as a potential candidate to regulate brain aging by normalizing dysregulated gene expression in aged astrocytes.

This study introduced an innovative nanozyme system called MCP@G, which was shown to improve diabetic wound healing in rats by alleviating mitochondrial oxidative stress, enhancing fibroblast migration, and promoting blood vessel and hair follicle regeneration, offering a promising approach for treating challenging diabetic wounds.

This review discusses the role of reactive oxygen species in wound healing, highlighting potential strategies like mitochondrial-targeted antioxidants for managing non-healing chronic wounds, and reports no new clinical results.

This study found that oxidative damage is present in the mitochondria of PolG mice, which exhibit premature aging-like phenotypes due to mitochondrial dysfunction.

This study found that transient mtDNA double strand breaks in mice accelerated aging in certain tissues through increased reactive oxygen species, independent of p21/p53 pathway mediation.

This review explores the roles of superoxide dismutases in cellular processes and cancer, highlighting the potential of SOD mimetics in enhancing cancer treatment strategies, but it reports no new clinical findings.

This study demonstrated that dominant mutations in mouse gasdermin A3 disrupt mitochondrial oxidative stress regulation, suggesting a gain-of-function effect on epidermal differentiation.

This study found that minoxidil provides cardioprotective effects in guinea-pig heart cells through selective activation of mitochondrial ATP-sensitive potassium channels.

This review examines the role of androgens and androgen receptors in regulating glucose and lipid metabolism, focusing on their effects on mitochondrial content and function; it also discusses the sex-dimorphic influence of androgens and provides theoretical insights into their mechanisms.

This chapter discusses charnolopharmacotherapeutics for various medical conditions and suggests antioxidant-loaded nanoparticles may improve treatment by enhancing central nervous system delivery and inducing charnolophagy.

This study observed that patients with alopecia areata had significantly different levels of oxidative stress markers SOD and MDA compared to controls.

This source critically examines Bruce Ames's influential contributions to biochemistry, particularly his theories on oxidative stress and mitochondrial DNA damage in aging, while acknowledging current challenges to his work and highlighting his lasting impact on the fields of mutagen screening and public health.

HPT axis hormones boost mitochondrial function and growth in hair follicles, potentially aiding hair health.

This review discusses the role of antioxidants in managing oxidative skin damage and reports no new results, emphasizing the need for understanding their mechanisms, limitations, and risks for safe use.

In this study, copper was found to promote the proliferation of dermal papilla cells in Rex rabbits by maintaining the function of the cellular mitochondrial electron transport chain.

This article discusses the relationship between mitochondrial DNA damage and atherosclerosis, suggesting that mtDNA damage may increase plaque vulnerability independent of reactive oxygen species, but reports no new clinical results.

This study found that ACOD1 deficiency in dermal papilla cells promotes mitochondrial dysfunction and contributes to cellular senescence in androgenetic alopecia, suggesting ACOD1 as a potential therapeutic target and 4-octyl itaconate as a promising treatment option for AGA.

In this study, treatment with finasteride altered the expression patterns of antioxidant enzymes in the epididymis of rats, potentially affecting its protective function for spermatozoa.

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.

In this study, Cyanidin 3-O-arabinoside was found to protect against DHT-induced dermal papilla cell senescence and mitochondrial dysfunction in androgenetic alopecia, restoring hair growth in mouse models.

This study found that knocking down SFRP2 in an AGA model improved hair regeneration and reduced cellular dysfunction, suggesting that targeting the SFRP2-FSTL1 axis could be a promising therapeutic strategy for androgenetic alopecia.

This study found that mitochondrial reactive oxygen species are crucial for normal epidermal differentiation and hair follicle growth, as demonstrated by impaired development in mice lacking these signals due to a keratinocyte-specific TFAM deficiency.

This study identified that copper depletion in dermal papilla cells reduced hair growth by boosting ROS levels, but ROS scavengers like NAC and ascorbic acid partially alleviated this effect.

This study found that treating mtDNA mutator mice with the antioxidant SkQ1 delayed aging traits and extended their lifespan, potentially by alleviating mitochondrial dysfunction caused by reactive oxygen species.

This review explores the mechanisms of hair cell death due to factors like noise, ototoxic drugs, and aging and reports no conclusive clinical results; ongoing research may eventually enable preventive treatments for hearing loss.

Healthy mitochondria in skin cells are essential for proper hair growth and skin cell interaction in mice.

In this study, researchers developed a wearable red and blue LED patch and a sprayable fibrin gel to treat infected wounds at home, demonstrating effective infection control and enhanced wound healing in diabetic mice and minipigs.

This review updates the protective effects and molecular mechanisms of melatonin against ultraviolet-induced damage in human skin, reporting no new clinical findings.

This study found that platelet-derived mitochondria can promote wound healing by reducing oxidative stress-induced apoptosis in vascular endothelial cells, with survivin identified as a potential target.

This review explores how low-energy He-Ne laser therapy may stimulate repigmentation in vitiligo by affecting mitochondrial pathways and melanocyte function, but does not report new clinical results.