ArticleHypertension (Dallas, Tex. : 1979)2026
Hypertension Drives Protein Lactylation and Vascular Dysfunction in Skeletal Muscle.
Milene T Fontes, Paul Townsend, Landon Butler, Juliana M Parente, Fênix A Araujo, Tiago J Costa, Gisele F Bomfim, Laena Pernomian, Wenbin Tan, Brandon N VanderVeen and 5 more
Abstract read
In one paragraphArticle in Hypertension (Dallas, Tex. : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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2 · The registryThe trial behind it
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
15 authors.
Milene T FontesCardiovascular 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.
Paul TownsendCardiovascular 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.
Landon ButlerDepartment of Physiological Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater (L.B., J.T.B.).ORCID 0000-0003-3299-0320 Juliana M ParenteCardiovascular 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.
Fênix A AraujoCardiovascular 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.ORCID 0000-0002-6063-1299 Tiago J CostaCardiovascular 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.ORCID 0000-0003-0780-4290 Gisele F BomfimCardiovascular 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.ORCID 0000-0001-5528-0028 Laena PernomianCardiovascular 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.ORCID 0000-0003-3930-0919 Wenbin TanCardiovascular 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.ORCID 0000-0002-2334-8988 Brandon N VanderVeenDepartment of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia (B.N.V., E.A.M.).ORCID 0000-0002-4535-0544 E Angela MurphyDepartment of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia (B.N.V., E.A.M.).
Joshua T ButcherDepartment of Physiological Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater (L.B., J.T.B.).ORCID 0000-0002-7341-1949 Cameron G McCarthyCardiovascular 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.ORCID 0000-0002-1380-779X Camilla F WenceslauCardiovascular 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.ORCID 0000-0002-0815-3568 Funding
Formyl peptide receptor activation induces vascular plasticity and remodeling inhypertensionR01HL149762 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · 2022 to 2025
$1.5MReprogramming endothelial cells to prevent and treat Alzheimer disease (AD) and HypertensionR21AG085331 · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · 2025 to 2025
$186kNHLBI NIH HHS R01 HL149762NIA NIH HHS R21 AG085331NIGMS NIH HHS R35 GM138191
6 · The paper itselfAbstract
backgroundEmerging evidence suggests a critical interplay between skeletal muscle metabolism and vascular function in the context of hypertension. Elevated plasma lactate levels precede the onset of hypertension and are inversely associated with skeletal muscle mass, highlighting skeletal muscle atrophy and metabolic dysregulation as key contributors to cardiovascular dysfunction.
methodsMale and female Wistar rats and spontaneously hypertensive rats were studied. Skeletal muscle performance was evaluated using in vivo plantarflexion torque measurements. Femoral arteries with surrounding skeletal muscle were isolated to assess contractility and relaxation. Plasma and muscle lactate levels were quantified using colorimetric assays. Structural remodeling and mitochondrial function were assessed via wheat germ agglutinin staining, succinate dehydrogenase activity, and high-resolution respirometry. Protein lactylation was evaluated by mass spectrometry-based lactylated proteomics. Human translational relevance was examined using publicly available skeletal muscle transcriptomic data.
resultsSpontaneously hypertensive rats exhibited skeletal muscle dysfunction marked by increased fatigability, reduced muscle mass, impaired mitochondrial activity, and elevated muscle lactate levels. Despite upregulation of oxidative markers, persistent lactate accumulation suggested a maladaptive metabolic shift. Proteomics revealed differential lactylation of key structural proteins (myosins, nebulin) and metabolic enzymes (Nampt, GAPDH [glyceraldehyde-3-phosphate dehydrogenase]). The anticontractile effect of skeletal muscle on femoral arteries was completely lost in spontaneously hypertensive rats, accompanied by impaired vascular relaxation and increased arterial lactylation. Human transcriptomic data supported parallel metabolic alterations in hypertension.
conclusionsHypertension disrupts skeletal muscle metabolic homeostasis and muscle-vascular communication, driven in part by persistent lactate accumulation and altered protein lactylation. Targeting lactate-mediated signaling may offer new therapeutic avenues for hypertensive vascular dysfunction.
Indexed as
HypertensionLactic AcidMuscle ProteinsMuscle, SkeletalAnimalsDisease Models, AnimalFemaleFemoral ArteryHumansMaleProteomicsRatsRats, Inbred SHRRats, WistarLactic AcidMuscle Proteinsarterieshypertensionmuscle, skeletalpost-translational, metabolism
Identifiers
PMID42017232
PMCPMC13105269
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