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This study found that removing PPARγ specifically from mouse adipose tissue led to severe fat loss, insulin resistance, diabetes, and associated metabolic abnormalities.

This study found that maternal PPARγ is essential for preventing the production of inflammatory lipids in mouse milk, which can otherwise cause inflammation, alopecia, and growth retardation in nursing pups.

This study found that PPAR alpha, -delta, and -gamma are expressed in human hair follicle cells, and clofibrate exhibited a beneficial effect on hair follicle survival in culture within a specific concentration range.

This study found that the selective PPARγ modulator GMG-43AC may inhibit unwanted hair growth by inducing catagen phase while preserving hair follicle epithelial progenitor cells, suggesting potential in anti-hirsutism therapy.

This review synthesizes current research on PPAR-γ signaling in hair follicle biology and its potential role in treating hair growth disorders like scarring alopecia and hirsutism, but reports no new clinical results.

This study found that loss of epidermal PPARγ in mice altered the expression of many genes related to skin inflammation, keratinization, and sebaceous gland function, indicating its key role in maintaining skin homeostasis.

This study found that the retinoid receptor and PPAR pathway are involved in hair follicle miniaturization in androgenetic alopecia, alongside androgen receptors.

In this study, aleglitazar and its metabolite M6 were evaluated for safety in non-clinical settings, revealing organ-targeting effects common to PPAR agonists but no significant tumor increase in rat carcinogenicity studies, supporting progression to Phase 3 clinical trials.

This study found that individuals with homozygous loss-of-function mutations in PLAAT3 experience a novel type of partial lipodystrophy linked to defects in white adipose tissue differentiation and function.

In this study, human cell models of hair follicles showed that araliadiol, a plant-derived polyacetylene compound, promotes hair growth through the p38/PPAR-γ signaling pathway, suggesting its potential as a new drug candidate for alopecia treatment.

This study found that the PPARγ modulator NAC-GED-0507-Levo may protect hair follicles from chemotherapy-induced damage, potentially offering a strategy to address irreversible hair loss in cancer patients.

This study found that loss of the DNA methyltransferase Dnmt3a, but not Dnmt3b, increased carcinogen-induced squamous tumors in murine epidermis, with combined deletion leading to more aggressive and metastatic carcinomas.

The research found that while Dnmt3a and Dnmt3b are not necessary for skin homeostasis in mice, the loss of Dnmt3a increases squamous tumor formation from carcinogens, and combined deletion of both results in more aggressive and metastatic tumors.

This study suggests that decreased PPARgamma function may trigger the pathogenesis of lichen planopilaris, and PPARgamma-targeted therapy could be a potential treatment method.

This study found that neonatal Regulatory T cells are crucial for maintaining PPARγ signaling in hair follicles, which supports melanocyte stem cell function and skin pigmentation during early postnatal development.

This review discusses the role of PPARs in skin health, suggesting both potential benefits and adverse effects, but reports no new experimental results; the authors emphasize the need for more research to understand these pathways.

This review discusses the role of peroxisome proliferator-activated receptors and their agonists in dermatology but reports no new clinical results.

This study suggests PPAR isotypes play distinct roles in skin, influencing epidermal barrier formation, sebocyte differentiation, and lipid production, with potential implications for treating skin disorders.

This review discusses the role of PPAR-γ in the pathogenesis of primary cicatricial alopecia, including its involvement in lichen planopilaris and treatment trials using PPAR-agonists, and reports no new clinical results.

This study found that the absence of vitamin D receptor-mediated suppression of PPARγ expression causes hair loss in VDR-null mice.

This study found that PPARα agonists provided protective effects in mouse models of alopecia areata by promoting early reversal of the condition and inhibiting T effector cell function, indicating potential therapeutic value for this inflammatory condition.

This study found that hepatic KRT79 expression is regulated by PPARA and is significantly associated with liver stress, suggesting it may serve as a diagnostic marker for liver diseases.

This study found that astilbin downregulates effector CD4+ T cell activities through the CYP1B1/ROS/PPARγ pathway, suggesting its potential use in treating inflammation.

This study found that FAM19A5 acts as a negative regulator of wound healing by hindering keratinocyte migration and partially transitioning them between epithelial and mesenchymal states, suggesting that targeting the FAM19A5-PPARD-Snail axis could offer new therapeutic options for impaired wound repair.

The researchers reported that PPARβ/δ may influence the yak hair follicle cycle by modulating lipid metabolism in dermal papilla cells, with varying expression during different hair growth phases, affecting both lipid content and cell proliferation.

In this study, researchers performed the first integrated transcriptomic and proteomic analysis of scalp biopsies from male androgenetic alopecia patients, finding a significant association between PPAR signaling pathways and AGA, with ME1 identified as a key regulator in this process.

A specific RNA molecule blocks hair growth by affecting a protein related to hair loss conditions.

This study found that the PPAR-γ modulator AGED can reverse epithelial-mesenchymal transition in hair follicles affected by lichen planopilaris ex vivo, suggesting potential for treating scarring alopecias.

This study found that N-acetyl-GED may protect and partially rescue human hair follicles from experimentally-induced epithelial-mesenchymal transition ex vivo, suggesting its potential in treating scarring alopecias like lichen planopilaris.

This study found that Rap1 deficiency in mice may lead to telomere shortening, DNA damage, and impaired mitochondrial function, contributing to cardiac aging and dysfunction.