ArticleAging cell2023
Carnitine acetyltransferase deficiency mediates mitochondrial dysfunction-induced cellular senescence in dermal fibroblasts.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- From energy metabolic homeostasis to immune remodeling: the role and therapeutic potential of STING signaling in the tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- MTDH inhibits CrAT to promote mitochondrial damage in palmitic acid-induced renal tubular cells.Acta diabetologica · 2026Article
- Adiponectin and aging: Mechanistic insights, clinical paradox, and therapeutic horizons.Ageing research reviews · 2026Review
- Disrupted epigenetic regulation in human senile lentigines revealed by characterizing gene expression and DNA methylation alterations.Clinical epigenetics · 2026Article
- Mitochondrial dynamics in skin health and disease: energy, aging, and therapeutic perspectives.Burns & trauma · 2026Review
- The mitochondrial logic of inflammaging: how energy imbalance drives fibroblast SASP and tissue-specific aging.Frontiers in immunology · 2026Review
- Energy Metabolic Regulatory Materials Promote Wound Healing in Senescent Environment.Progress in molecular and subcellular biology · 2026Review
- Androgen Receptors Promote Oxidative Phosphorylation and Resistance to Palmitate Lipotoxicity in ER-Mutant Breast Cancer.Endocrinology · 2025Article
- Over-Represented Senescent Keratinocytes in Hyperpigmented Spots Promote Melanocyte Activation via IGFBP3 and NGF.International journal of molecular sciences · 2025Article
- Advanced glycation end products induce inflammaging in periodontal ligament fibroblasts through RAGE/AKT/mTOR/glycolysis pathway.Acta odontologica Scandinavica · 2025Article
- Quercetin alleviates acute pancreatitis by modulating glycolysis and mitochondrial function via PFKFB3 inhibition.Cellular and molecular life sciences : CMLS · 2025Article
- Review
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- CRAT downregulation promotes ovarian cancer progression by facilitating mitochondrial metabolism through decreasing the acetylation of PGC-1α.Cell death discovery · 2025Article
- Recent advances in dermal fibroblast senescence and skin aging: unraveling mechanisms and pioneering therapeutic strategies.Frontiers in pharmacology · 2025Review
- Predictive Biomarkers: A New Frontier in Bespoke Aesthetic Dermatology.Aesthetic surgery journal. Open forum · 2025Article
- Pterostilbene mitigates the senescence of human dermal fibroblast cells by enhancing mitochondrial quality.Frontiers in pharmacology · 2025Article
- Immune aging and infectious diseases.Chinese medical journal · 2024Review
- Beneficial Effects of Epigallocatechin Gallate in Preventing Skin Photoaging: A Review.Molecules (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is accompanied by impaired mitochondrial function and accumulation of senescent cells. Mitochondrial dysfunction contributes to senescence by increasing the levels of reactive oxygen species and compromising energy metabolism. Senescent cells secrete a senescence-associated secretory phenotype (SASP) and stimulate chronic low-grade inflammation, ultimately inducing inflammaging. Mitochondrial dysfunction and cellular senescence are two closely related hallmarks of aging; however, the key driver genes that link mitochondrial dysfunction and cellular senescence remain unclear. Here, we aimed to elucidate a novel role of carnitine acetyltransferase (CRAT) in the development of mitochondrial dysfunction and cellular senescence in dermal fibroblasts. Transcriptomic analysis of skin tissues from young and aged participants showed significantly decreased CRAT expression in intrinsically aged skin. CRAT downregulation in human dermal fibroblasts recapitulated mitochondrial changes in senescent cells and induced SASP secretion. Specifically, CRAT knockdown caused mitochondrial dysfunction, as indicated by increased oxidative stress, disruption of mitochondrial morphology, and a metabolic shift from oxidative phosphorylation to glycolysis. Mitochondrial damage induced the release of mitochondrial DNA into the cytosol, which activated the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) and NF-ĸB pathways to induce SASPs. Consistently, fibroblast-specific CRAT-knockout mice showed increased skin aging phenotypes in vivo, including decreased cell proliferation, increased SASP expression, increased inflammation, and decreased collagen density. Our results suggest that CRAT deficiency contributes to aging by mediating mitochondrial dysfunction-induced senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.