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January 1, 2023ResearchOpen Access

MAVS Antagonizes Human Stem Cell Senescence as a Mitochondrial Stabilizer

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Key result

Depletion of MAVS in human mesenchymal stem cells accelerated cellular senescence and mitochondrial dysfunction, which was alleviated by replenishing MAVS or OPA1.

Why the study?

It was unknown whether the mitochondrial antiviral signaling protein (MAVS) also regulates human stem cell senescence.

Does MAVS regulate human stem cell senescence and mitochondrial homeostasis?

Population

MAVS-knockout human stem cell models including human mesenchymal stem cells

Comparison

MAVS or OPA1 depletion vs replenishment in MAVS-knockout cells

Design

Preclinical in vitro laboratory study using CRISPR/Cas9-mediated gene editing

Authors

CWCui WangHebei Medical UniversityKYKuan YangXi'an Honghui HospitalXLXiaoqian LiuQingdao University

Discussion

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Implication

MAVS-OPA1 axis may modulate stem cell senescence; leaves open any role in human regenerative or aging therapies.

Key Points

  • This research explores how MAVS influences senescence in human stem cells and its role in mitochondrial function.
  • Used CRISPR/Cas9-mediated gene editing to create MAVS-knockout human stem cell models.
  • Directed differentiation techniques applied to evaluate cellular senescence in hMSCs.
  • Analyzed interactions between MAVS and the guanosine triphosphatase OPA1.
  • MAVS deficiency accelerated senescence phenotypes in hMSCs (p<0.05).
  • Depletion of MAVS or OPA1 led to mitochondrial dysfunction and increased senescence markers.
  • Replenishment of MAVS or OPA1 in knockout hMSCs alleviated mitochondrial defects and delayed senescence.

Structured PICO

Does MAVS regulate human stem cell senescence and mitochondrial homeostasis?

P
Population
Human mesenchymal stem cells (hMSCs) and various MAVS-knockout human stem cell models generated via CRISPR/Cas9-mediated gene editing and directed differentiation
I
Intervention
MAVS knockout (depletion) and replenishment of MAVS or OPA1
C
Comparator
Wild-type or non-knockout stem cells
O
Outcome
Cellular senescence phenotypes and mitochondrial structural integrity/functional homeostasissurrogate

MAVS plays an uncanonical role in safeguarding mitochondrial homeostasis and antagonizing human stem cell senescence through interaction with OPA1.

Cite This Study

Wang et al. (2023) studied Cellular senescence. MAVS-knockout via CRISPR/Cas9 vs. Wild-type or replenishment of MAVS/OPA1 was evaluated on Mitochondrial structural integrity, functional homeostasis, and cellular senescence. Depletion of MAVS in human mesenchymal stem cells accelerated cellular senescence and mitochondrial dysfunction, which was alleviated by replenishing MAVS or OPA1.

synapsesocial.com/papers/6a21111dbbda06802a96794fhttps://doi.org/10.34133/research.0192
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Also Consider

Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1A biomarker that identifies senescent human cells in culture and in aging skin in vivo.1995 · 7,598 citations
  2. 2Stabilization of heterochromatin by CLOCK promotes stem cell rejuvenation and cartilage regeneration2020 · 111 citations