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This research investigates apoptosis and bcl 2 expression in hair follicles cultured with and without biotin, but it reports no new results.

This study found that Yangxuebushen Decoction significantly promoted hair regrowth and improved hair follicle structure in a cyclophosphamide-induced alopecia mouse model by reducing inflammation, oxidative stress, and apoptosis.

In this study, researchers linked SARS-CoV-2 infection to telogen effluvium in some COVID-19 patients by observing the accumulation of viral proteins in hair follicle cells, which may trigger stress responses and cell death, suggesting hair follicles as a potential target in COVID-19.

This study suggests that Bim and Puma proteins play a role in hair follicle development and maintenance, although they only partially overlap with apoptosis during normal hair cycle stages.

This study suggests that the anti-inflammation and anti-oxidation properties of Taohong Siwu decoction may be linked to its effects on androgenic alopecia through specific biological processes and pathways.

This practical guide introduces methods to study human dermal white adipose tissue but does not report new clinical results, emphasizing available techniques and staining protocols.

This study suggests that Hejie Shengfa Decoction may help treat alopecia areata by influencing immune and inflammatory pathways, regulating apoptosis, and enhancing the follicular microenvironment.

This study found that the topical Shen Bai hair growing decoction may improve androgenetic alopecia in mice by suppressing TNF-α and IL-6 levels, enhancing follicle density, and reducing apoptosis.

This study found that cyclophosphamide induced significant keratinocyte apoptosis in anagen hair follicles of mice, while topical calcitriol-analogs reduced this apoptosis, suggesting a protective effect against chemotherapy-induced alopecia.

This study observed that gamma-ray induced apoptosis in ICR mouse hair follicles could be reduced by pretreatments with diethyldithiocarbamate or green tea, suggesting these agents as potential radioprotectors.

This study explores the correlation between sirtuins' expression, histone deacetylation, and redox status in young and old monozygotic twins to understand their role in age-related mechanisms.

This study suggests that low proliferation rates in bald areas of androgenetic alopecia patients, along with persistent inflammatory infiltrate, may lead to follicular miniaturization and fibrosis.

This study found that PBX1 enhances the proliferation and reprogramming of hair follicle mesenchymal stem cells by activating the AKT/GSK3β signaling pathway, promoting NANOG expression, and inhibiting apoptosis.

This study found significant differences in bcl-2 expression between areas of the scalp affected and unaffected by androgenetic alopecia, suggesting a uniform follicle population or synchronized follicular cycling in affected areas.

This study found that PBX1 overexpression reduces hair follicle-derived mesenchymal stem cell senescence and apoptosis by interacting with SIRT1 and PARP1, highlighting a potential mechanism for addressing aging-related diseases.

This study observed that a topical liposome formulation of a 5‐α‐reductase inhibitor effectively reduced the size of treated sebaceous glands and induced apoptosis in a hamster model, suggesting potential benefits for acne treatment.

This study found that nicotine caused damage to cochlear hair cells in vitro, and melatonin might protect against this damage, indicating its potential as a treatment for smoking-induced hearing loss.

In this study, the researchers identified a PBX1-SIRT1-PARP1 axis that plays a crucial role in reducing senescence and apoptosis in hair follicle-derived mesenchymal stem cells.

This study found that diffuse alopecia in HIV-1-infected patients is characterized by higher rates of follicular stem cell apoptosis compared to controls, suggesting a hair cycle disturbance associated with the infection.

This study found that testosterone and 5α-dihydrotestosterone induced apoptosis in dermal papilla cells from nonbalding scalp regions, suggesting a high androgen stimulus can trigger cell death related to androgenetic alopecia.

This study isolated a bioactive peptide from Trapa japonica fruit and found that it may protect human dermal papilla cells from DHT-induced stress, suggesting potential for biomedical applications.

This study found that cyclosporine A's enhancement of hair growth in mice is partly due to its ability to block the nuclear translocation of apoptosis-inducing factor, slowing the hair follicle transition to the catagen phase.

This study found that PM2.5 exposure induced oxidative stress in human keratinocytes and mouse skin, causing cellular damage, which was mitigated by the antioxidant N-acetyl cysteine.

The researchers reported that DHT-inducible DKK-1 may play a significant role in DHT-driven balding by inhibiting hair follicle cell growth and promoting apoptosis in androgenetic alopecia.

This review suggests that isotretinoin's effects on severe acne and various cancers may result from apoptosis, which might also explain its adverse effects through genetic variability.

This study reports that overexpressing the BMP antagonist noggin in mice inhibits eyelid opening by reducing apoptosis and delaying cell differentiation in the eyelid epithelium.

This study found that overexpressing human Bcl-2 in mice protected epidermal keratinocytes from UVB-induced apoptosis but unexpectedly increased apoptosis during hair follicle regression and chemotherapy.

The study found that melatonin treatment in early postnatal cashmere goats increased both the quantity and quality of cashmere by promoting secondary hair follicle development and enhancing antioxidant enzyme activities.

In this study, photodynamic therapy significantly reduced inflammatory acne lesions and sebum secretion, possibly by inducing apoptosis in sebaceous glands and down-regulating TLR-2 and TLR-4 expression.

Long-term use of a certain medication can worsen erectile function in aged rats by damaging penile muscle cells.