research The Dual Nature of Cellular Senescence: From Aging Signature to Regenerative Catalyst
Cellular senescence can both hinder and promote hair growth, suggesting new ways to treat hair loss.
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840-870 / 1000+ results research 652 Short cell cycle duration is a phenotype of human epidermal stem cells
research Novel anti-aging gene NM_026333 contributes to proton-induced aging via NCX1-pathway
The gene NM_026333 slows down aging by affecting the NCX1 pathway and could be targeted for anti-aging treatments.
research Spontaneous Squamous Cell Carcinoma Induced by the Somatic Inactivation of Retinoblastoma and Trp53 Tumor Suppressors
Inactivating both p53 and Rb genes in mice speeds up aggressive skin cancer development.
research 692 Prevention of H 2 O 2 -induced cellular senescence in human hair follicle dermal papilla cells
Certain compounds can protect hair cells from aging and promote growth.
research 138: Induction of cellular senescence and hair follicle stem cell dysfunction upon p14ARF and p16Ink4a expression in the skin
p14ARF and p16Ink4a cause hair follicle stem cell aging and dysfunction.
research Progressive Alopecia Reveals Decreasing Stem Cell Activation Probability during Aging of Mice with Epidermal Deletion of DNA Methyltransferase 1
Mice lacking a key DNA methylation enzyme in skin cells have a lower chance of activating stem cells necessary for hair growth, leading to progressive hair loss.
research Data from Spontaneous Squamous Cell Carcinoma Induced by the Somatic Inactivation of Retinoblastoma and Trp53 Tumor Suppressors
Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.
research Hair follicle aging is driven by transepidermal elimination of stem cells via COL17A1 proteolysis
Hair loss is caused by the breakdown of a protein called COL17A1 in hair follicle stem cells.
research Data from Spontaneous Squamous Cell Carcinoma Induced by the Somatic Inactivation of Retinoblastoma and Trp53 Tumor Suppressors
Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.
research Senescence-induced reparative fibroblasts enable scarless wound healing in aged murine skin.
Older mice heal wounds without scars due to special fibroblasts.
research Metabolic and transcriptomic reprogramming during contact inhibition-induced quiescence is mediated by YAP-dependent and YAP-independent mechanisms
Quiescent cells have increased mitochondrial activity and ECM gene expression, but reduced glycolysis.
research The G1/S transition in mammalian stem cellsin vivois autonomously regulated by cell size
Cell size independently controls when stem cells divide.
research 090 Reactive lipids from the secretome of senescent fibroblasts modify the extracellular matrix with functional consequences for resident cells
Reactive lipids from aging cells change the extracellular matrix, affecting cell function and inflammation.
research Aging in the sebaceous gland
Sebaceous glands age due to genetic and environmental factors, affecting sebum production and composition.
research Ginsenoside Rb1 retards aging process by regulating cell cycle, apoptotic pathway and metabolism of aging mice
Ginsenoside Rb1 slows down aging in mice by affecting cell growth, cell death, and metabolism.
research Intracellular protons accelerate aging and switch on aging hallmarks in mice
Acid inside cells speeds up aging and turns on aging signs in mice.
research Accelerated senescence in skin in a murine model of radiation-induced multi-organ injury
High-dose radiation speeds up aging in skin stem cells.
research Cellular plasticity in reprogramming, rejuvenation and tumorigenesis: a pioneer TF perspective
Controlling cellular changes can enable safe rejuvenation without cancer risk.
research Microarray analysis of androgenetic and senescent alopecia: Comparison of gene expression shows two distinct profiles
The conclusion is that androgenetic alopecia and senescent alopecia have unique gene changes, suggesting different causes and potential treatments for these hair loss types.
research RNase L represses hair follicle regeneration through altered innate immune signaling
RNase L hinders hair follicle regeneration by altering immune signals.
research Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark
The most common sign of aging at the gene level is more Ectodysplasin A2 Receptor (EDA2R) being made.
research 244 Defective maintenance of hair follicle stem cells through COL17A1 loss orchestrates the hair follicle aging program
Loss of COL17A1 causes hair follicle stem cells to age and leads to hair loss.
research 1360 Fate tracing of DNA-damaged hair follicle stem cells and their seno-differentiation clearance out of the niche
Damaged hair follicle stem cells may leave the skin to help maintain youthfulness.
research 0871 Skin longevity breakthroughs and targets for cellular age reversal: Sirtuins, key epigenetics regulators
research Gorab deficiency in skin dermis accelerates aging and is associated with dysregulation of RCHY1 ‐mediated P53 ubiquitination
Gorab deficiency speeds up skin aging by disrupting protein regulation and reducing collagen.
research Faculty Opinions recommendation of Conditional telomerase induction causes proliferation of hair follicle stem cells.
Activating telomerase can boost hair follicle stem cell growth and hair production.
research Ageing and colony-forming efficiency of human hair follicle keratinocytes
Aging reduces the ability of human hair follicle cells to form new cell colonies.
research Genetics of Progeria and Aging
Progeria, a disease that causes early aging, is linked to a gene mutation and helps us understand normal aging.
research A Wnt5a-Cdc42 axis controls aging and rejuvenation of hair-follicle stem cells
Aging-related changes in hair follicle stem cells can be partially reversed with a specific treatment.