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TRPM7 Deficiency Accelerates Vascular Senescence by Inhibiting H3K18 Lactylation.

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Area of Science:

  • Molecular Biology
  • Aging Research
  • Vascular Biology

Background:

  • Blood vessels are vulnerable to aging, with vascular endothelial cells playing a key role in this process.
  • The precise molecular mechanisms driving vascular endothelial aging are not fully understood.

Purpose of the Study:

  • To identify key molecular players in vascular endothelial aging.
  • To elucidate the mechanisms by which TRPM7 influences vascular aging.
  • To explore potential therapeutic interventions for vascular anti-aging.

Main Methods:

  • Investigated the role of TRPM7 in mouse models with endothelial-specific TRPM7 deletion.
  • Analyzed molecular changes including lactate production, p300 activity, and histone H3K18 lactylation.
  • Examined gene expression profiles related to senescence and angiogenesis.
  • Tested interventions such as p21 inhibition and lactate supplementation.

Main Results:

  • Endothelial TRPM7 deletion accelerated premature vascular aging in mice.
  • TRPM7 deficiency led to reduced lactate production, decreased p300 activity, and lower histone H3K18 lactylation.
  • This resulted in increased p21 (senescence) and decreased angiogenesis gene expression.
  • Inhibition of p21 or lactate supplementation reversed the accelerated aging phenotype.

Conclusions:

  • TRPM7 is a critical regulator of vascular endothelial aging.
  • The TRPM7-lactylation axis (specifically H3K18la) is a key mechanism in vascular aging.
  • Targeting the TRPM7-H3K18la pathway offers potential for novel vascular anti-aging therapies.