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Taxane chemotherapy can cause permanent hair loss by damaging hair follicles and altering their DNA.

This study suggests that myotonic dystrophies may qualify as segmental progeroid disorders due to molecular and clinical similarities with typical progeroid syndromes.

This review discusses how the nuclear lamina integrates biochemical and mechanical signals to influence gene expression and skin homeostasis, but reports no new clinical results.

Paclitaxel chemotherapy causes premature aging and damage to hair follicles, potentially leading to permanent hair loss.

This review discusses the role of lamins in development, tissue maintenance, and stress response, and does not report new experimental findings.

This review discusses genetic mutations associated with Hutchinson-Gilford progeria syndrome and reports no clinical results; the authors emphasize the importance of cardiovascular monitoring in management.

This review explores how cell and mouse models have contributed to understanding the mechanisms of human aging, particularly focusing on Hutchinson-Gilford Progeria Syndrome, and reports no new clinical results.

In this study, norgalanthamine was found to stimulate hair growth in cultured rat dermal papilla cells by activating the ERK 1/2, PI3K/AKT, and Wnt/β-catenin signaling pathways.

This study found that the interaction between heat shock protein 90 and lamin A/C is crucial for the growth, migration, and self-aggregation of dermal papilla cells, suggesting a potential role in alopecia areata mechanisms.

This study found that mackerel-derived fermented fish oil extract and its component DHA promote hair growth by activating anagen pathways in dermal papilla cells.

This review discusses the interplay between signaling/transcription factor-mediated and epigenetic mechanisms in skin development and regeneration, highlighting the need for further exploration of epigenome reorganization in these processes.

This study found that keratin 17 and TNFα play interdependent roles in regulating hair follicle cycling, with TNFα required for the anagen–catagen transition and its ablation partially rescuing hair cycling defects in K17-null mice.

This study suggests that crosstalk between Wnt/β-catenin and TGF-β signaling pathways may contribute to the development of androgenetic alopecia.

This review highlights various methods of stem cell communication that reflect the unique organization and function of different tissues and reports no new results.

This study found that although progerin expression in mouse skin causes significant nuclear shape changes in keratinocytes, it does not result in alopecia or common skin abnormalities seen in human Hutchinson–Gilford progeria syndrome.

This study found that intermittent treatment with FTI lonafarnib and sulforaphane may be a promising therapeutic approach for children with Hutchinson-Gilford progeria syndrome, as it improved the cellular phenotype.

This review discusses the similarities between myotonic dystrophy and aging, highlighting the role of cellular senescence in its pathophysiology, and reports no new clinical findings; the authors note potential anti-aging therapy applications.

This study reported that inhibiting the JAK-STAT pathway with baricitinib restored cellular homeostasis, delayed senescence, and reduced proinflammatory markers in Hutchinson-Gilford progeria syndrome cell models.

This review summarizes recent findings on keratins 6, 16, and 17, highlighting their role in keratinocyte behavior and nuclear functions, and discusses their potential as biomarkers for various skin pathologies, including damage, inflammation, and cancer, rather than in healthy skin.

In a study using a mouse model of diabetes, chitosan-based hydrogels increased healing markers and improved wound closure and tissue repair compared to untreated wounds, but human efficacy needs further validation.

This study used molecular docking simulations to identify Adapalene, Diosmin, and Azelastine as promising drugs for repurposing against onchocerciasis by targeting proteins in the parasite and its endosymbiont; further research is needed to confirm their efficacy.

This study found that dihydrotestosterone (DHT) may shorten the hair growth cycle through mechanisms like cell-cycle arrest and β-catenin downregulation in rat hair follicle cells.

Acankoreoside J from Acanthopanax koreanum may help promote hair growth.

In this study, overexpression of YAP1 was found to promote adipogenic differentiation of goat adipose-derived mesenchymal stem cells by up-regulating LATS2 expression and activating the Hippo pathway's negative feedback loop.

This study found that Sargassum muticum extract and apo-9′-fucoxanthinone promoted hair growth in rat and mouse models by increasing dermal papilla cell proliferation and activating certain signaling pathways.

This study found that keratin 15 lacks the ability to sequester YAP1 in keratinocytes effectively, unlike keratin 14, and suggests that a higher K15:K14 ratio may promote a progenitor state and inhibit differentiation in epidermal keratinocytes.

This study observed a significant increase in cellular retinol-binding protein-1 expression in lesional skin of patients with alopecia areata compared to healthy controls, suggesting its potential role in the disease's pathogenesis.

In a neonatal rat model, this study found that topical CDK2 inhibitors reduced chemotherapy-induced hair loss in 33 to 50% of the animals, suggesting a potential strategy for preventing alopecia in cancer patients.

This study reports a novel geometric medicine solution, N‑K GM SERIES, claiming to eliminate aflatoxin, offer a universal cancer cure, and provide numerous health benefits, including increased life expectancy, with deployment focused on the "Aflatoxin Belt" regions like Sudan.

In this study, a novel geometric medicine approach, utilizing the N-K Universal Computer, was reported to eliminate aflatoxin contamination and significantly reduce cancer rates across the "Aflatoxin Belt" through precision targeting of harmful fungi while preserving ecological balance, without observed toxicity or resistance.