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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 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.

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 schizophrenia-derived neurons exhibited impaired differentiation and mitochondrial dysfunction, suggesting a potential link between these factors and neurodevelopmental processes in schizophrenia.

This review discusses the role of mitochondria and evaluates methodologies for assessing mitochondrial function and toxicity, particularly in the context of HIV and antiretroviral treatments, but it reports no new empirical findings.

In this study, researchers found that the absence of type I or type II keratins in mice leads to severe skin barrier defects, highlighting keratins' crucial role in epidermal structure and function.

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

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 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 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.

In this study, researchers found that depleting mtDNA in mice caused skin wrinkles and hair loss but restoring mitochondrial function reversed these effects, highlighting mtDNA's significant role in skin and hair health.

This study found that ZDHHC13 deficiency in mice is associated with abnormal liver function, lipid metabolism issues, and impaired mitochondrial function, highlighting ZDHHC13's regulatory role in liver metabolism.

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

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 observed that partial autotaxin deficiency in mice protects against diet-induced obesity and systemic insulin resistance, suggesting the ATX-LPA pathway negatively affects skeletal muscle insulin signaling and mitochondrial function during obesity.

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 study visualized mitochondrial metabolism in cultured bovine hair follicles and plucked human hairs, finding that ROS and mitochondrial polarization correlate in specific hair follicle regions, particularly near keratin deposition sites.

This study found significant variation in tissue mutant load in individuals with the T8993G mutation, which complicates genetic counseling and may inform genotype-phenotype correlations, especially using hair bulb mtDNA analysis.

This study found that novel MPC inhibitor analogues with specific chemical modifications promoted significant hair growth in shaved mice when applied topically.

This study found that β-sitosterol, a brain-penetrable phytosterol, reduced melanoma cell growth and brain metastasis formation by interfering with mitochondrial respiration, suggesting its potential as an adjuvant therapy to BRAF inhibitors for patients with melanoma brain metastases.

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

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.

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 found that liposterolic extracts of Serenoa repens enhanced hair regeneration and repair in DHT-induced hair loss mouse models, suggesting potential effects comparable to finasteride.

This study found that minoxidil prevents long-term serotonergic toxicity induced by MDMA in rats, primarily by opening mitochondrial KATP channels and involving Akt and MAP kinases in its neuroprotective mechanism.

This study found that the PPAR-γ modulator N-acetyl-GED may enhance mitochondrial function in human hair follicles, particularly in outer root sheath keratinocytes.

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 dutasteride reduced β-amyloid plaque load in a cerebral amyloidosis model, seemingly linked to mitochondrial apoptosis and autophagy processes.

This study found that metabolism-related genes significantly impact the prognosis and metastasis in breast cancer, and the development of prediction models may guide personalized therapeutic strategies.

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.