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Hypertension Drives Protein Lactylation and Vascular Dysfunction in Skeletal Muscle.

Milene T Fontes1, Paul Townsend1, Landon Butler2

  • 1Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy (M.T.F., P.T., J.M.P., F.A.A., T.J.C., G.F.B., L.P., W.T., C.G.M., C.F.W.), University of South Carolina, Columbia.

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Hypertension impairs skeletal muscle function and vascular health due to lactate buildup and altered protein lactylation. Addressing lactate signaling may offer new treatments for hypertensive vascular dysfunction.

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Area of Science:

  • Cardiovascular Physiology
  • Skeletal Muscle Metabolism
  • Vascular Biology

Background:

  • Hypertension is linked to skeletal muscle atrophy and metabolic issues.
  • Elevated plasma lactate and reduced muscle mass precede hypertension onset.
  • Skeletal muscle dysfunction contributes to cardiovascular problems.

Purpose of the Study:

  • Investigate the link between skeletal muscle metabolism and vascular function in hypertension.
  • Determine the role of lactate accumulation and protein lactylation in hypertensive vascular dysfunction.

Main Methods:

  • Studied Wistar and spontaneously hypertensive rats.
  • Assessed skeletal muscle performance, vascular contractility, and relaxation.
  • Quantified lactate levels and mitochondrial function.
  • Analyzed protein lactylation via proteomics and human transcriptomic data.

Main Results:

  • Hypertensive rats showed muscle dysfunction, increased fatigability, and elevated muscle lactate.
  • Lactate accumulation persisted despite oxidative marker upregulation.
  • Differential protein lactylation observed in structural and metabolic proteins.
  • Lost anticontractile effect of skeletal muscle on arteries, with impaired vascular relaxation and increased arterial lactylation.

Conclusions:

  • Hypertension disrupts skeletal muscle metabolism and muscle-vascular communication via lactate accumulation and protein lactylation.
  • Targeting lactate-mediated signaling presents potential therapeutic strategies for hypertensive vascular dysfunction.