ArticleJournal of biomedical science2022
Cyanidin 3-O-arabinoside suppresses DHT-induced dermal papilla cell senescence by modulating p38-dependent ER-mitochondria contacts.
Article in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Tolerogenic dendritic cell-conditioned medium promotes hair growth by modulating follicular microenvironment in a DHT-treated mouse model.Molecular and cellular biochemistry · 2026Article
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Aging of hair follicle stem cells and their niche: mechanisms and regenerative therapeutic strategies.Cell communication and signaling : CCS · 2026Review
- hUC-MSC-exosomes deliver Let-7b/7f-5p to dermal papilla cells for a multi-target synergistic treatment of androgenetic alopecia.Journal of nanobiotechnology · 2026Article
- Polygonatum polysaccharide microspheres encapsulated living Clostridium butyricum for mucosal barrier repair and immune regulation.Journal of nanobiotechnology · 2026Article
- Development and validation of a comprehensive in vitro organ model for androgenetic alopecia.BMC biotechnology · 2026Article
- Dual-drug nanostructured lipid carriers of spironolactone and 2-deoxy-D-ribose for targeted follicular delivery in androgenetic alopecia.Drug delivery and translational research · 2026Article
- ACOD1 deficiency promotes DDX1 methylation-mediated mitochondrial dysfunction and dermal papilla cell senescence in androgenetic alopecia.BMC medicine · 2026Article
- Ageing-Dependent Thyroid Hormone Receptor α Reduction Activates IP3R1-Meditated CaCell proliferation · 2026Article
- Amine-Functionalized Chitosan/dECM Composite Promotes Cutaneous Regeneration and Hair Follicle Activation by Regulating Oxidative Stress and Inflammation.Advanced healthcare materials · 2026Article
- Role of ASLNC168501 in regulating hair follicle stem cell activity via the AR/miR-128-3p/IGF-1 pathway.Stem cell research & therapy · 2026Article
- Sesamin alleviates androgenetic alopecia by targeting the AR MAPK Wnt axis.Scientific reports · 2026Article
- Oxidative Stress and Hormone-Regulated Dermal Papilla Cell-Targeted Nanomodulators: Reverse Cellular Senescence for Androgenetic Alopecia Therapy.Biomaterials research · 2026Article
- Rejuvenating senescent hair follicles: a novel conjugated linoleic acid based nanovesicle approach to treat androgenic alopecia.Journal of nanobiotechnology · 2025Article
- Phytochemicals for Hair Health Targeting Growth Signaling Molecules in Hair Follicular Stem Cells: A New Strategy for Hair Growth.Journal of microbiology and biotechnology · 2025Review
- NOX2 Contributes to High-Frequency Outer Hair Cell Vulnerability in the Cochlea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Single-Cell RNA Sequencing Highlights a Contribution of Human Amniotic Mesenchymal Stem Cells-Derived Exosomes to Androgenetic Alopecia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- CXCL12 Drives Reversible Fibroimmune Remodeling in Androgenetic Alopecia Revealed by Single-Cell RNA Sequencing.International journal of molecular sciences · 2025Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAndrogenetic alopecia (AGA) is a genetic disorder caused by dihydrotestosterone (DHT), accompanied by the senescence of androgen-sensitive dermal papilla cells (DPCs) located in the base of hair follicles. DHT causes DPC senescence in AGA through mitochondrial dysfunction. However, the mechanism of this pathogenesis remains unknown. In this study, we investigated the protective role of cyanidins on DHT-induced mitochondrial dysfunction and DPC senescence and the regulatory mechanism involved.
methodsDPCs were used to investigate the effect of DHT on mitochondrial dysfunction with MitoSOX and Rhod-2 staining. Senescence-associated β-galactosidase activity assay was performed to examine the involvement of membrane AR-mediated signaling in DHT-induced DPC senescence. AGA mice model was used to study the cyanidins on DHT-induced hair growth deceleration.
resultsCyanidin 3-O-arabinoside (C3A) effectively decreased DHT-induced mtROS accumulation in DPCs, and C3A reversed the DHT-induced DPC senescence. Excessive mitochondrial calcium accumulation was blocked by C3A. C3A inhibited p38-mediated voltage-dependent anion channel 1 (VDAC1) expression that contributes to mitochondria-associated ER membrane (MAM) formation and transfer of calcium via VDAC1-IP3R1 interactions. DHT-induced MAM formation resulted in increase of DPC senescence. In AGA mice models, C3A restored DHT-induced hair growth deceleration, which activated hair follicle stem cell proliferation.
conclusionsC3A is a promising natural compound for AGA treatments against DHT-induced DPC senescence through reduction of MAM formation and mitochondrial dysfunction.
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