ArticleResearch (Washington, D.C.)2023
MAVS Antagonizes Human Stem Cell Senescence as a Mitochondrial Stabilizer.
Article in Research (Washington, D.C.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Systematic review and meta-analysis of antioxidants with or without exercise training improving muscle condition in older adults.Scientific reports · 2025Pooled it
- Rejuvenation of Bone Marrow Mesenchymal Stem Cells: Mechanisms and Their Application in Senile Osteoporosis Treatment.Biomolecules · 2025Pooled it
- Review
- MAVS/CMTM6 axis couples mitochondrial homeostasis to immunogenic senescence via CCL3-driven T-cell recruitment in renal carcinoma.Journal for immunotherapy of cancer · 2025Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025Review
- AI-identified CD133-targeting natural compounds demonstrate differential anti-tumor effects and mechanisms in pan-cancer models.EMBO molecular medicine · 2025Article
- Metabolic regulation in the senescence process of stem cells.Stem cells translational medicine · 2025Review
- Mitochondrial sirtuins, key regulators of aging.Life medicine · 2025Review
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- SLC6A6-Mediated Taurine Uptake Sustains Corneal Epithelial Stem/Progenitor Cell Function to Counteract Age-Related Dysfunction.Investigative ophthalmology & visual science · 2025Article
- RIG-I-driven CDKN1A stabilization reinforces cellular senescence.Science China. Life sciences · 2025Article
- Targeting NAMPT-OPA1 for treatment of senile osteoporosis.Aging cell · 2025Article
- From mitochondria to heart: the role and challenges of mitochondrial antiviral signaling protein in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- HOXC10 Protects from Skin Aging by Targeting the FZD6/Wnt/β-Catenin Signaling Pathway.Research (Washington, D.C.) · 2025Article
- CRISPR screening uncovers nucleolar RPL22 as a heterochromatin destabilizer and senescence driver.Nucleic acids research · 2024Article
- Single-nucleus transcriptomics uncovers a geroprotective role of YAP in primate gingival aging.Protein & cell · 2024Article
- A new perspective on prostate cancer treatment: the interplay between cellular senescence and treatment resistance.Frontiers in immunology · 2024Review
- Mitophagy Promotes Hair Regeneration by Activating Glutathione Metabolism.Research (Washington, D.C.) · 2024Article
- Migrasomes trigger innate immune activation and mediate transmission of senescence signals across human cells.Life medicine · 2023Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is a hallmark feature of cellular senescence and organ aging. Here, we asked whether the mitochondrial antiviral signaling protein (MAVS), which is essential for driving antiviral response, also regulates human stem cell senescence. To answer this question, we used CRISPR/Cas9-mediated gene editing and directed differentiation techniques to generate various MAVS-knockout human stem cell models. We found that human mesenchymal stem cells (hMSCs) were sensitive to MAVS deficiency, as manifested by accelerated senescence phenotypes. We uncovered that the role of MAVS in maintaining mitochondrial structural integrity and functional homeostasis depends on its interaction with the guanosine triphosphatase optic atrophy type 1 (OPA1). Depletion of MAVS or OPA1 led to the dysfunction of mitochondria and cellular senescence, whereas replenishment of MAVS or OPA1 in MAVS-knockout hMSCs alleviated mitochondrial defects and premature senescence phenotypes. Taken together, our data underscore an uncanonical role of MAVS in safeguarding mitochondrial homeostasis and antagonizing human stem cell senescence.
Identifiers
What OpenQuestion holds
Registered trials
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.