ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Hyperhomocysteinemia attenuates angiogenesis through reduction of HIF-1α and PGC-1α levels in muscle fibers during hindlimb ischemia.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Uncovering Hyperhomocysteinemia: Global Risk Patterns and Molecular Disruption in Brain and Vascular Health.Journal of neurochemistry · 2025Review
- Homocysteine exchange across skeletal muscle in patients with chronic kidney disease.Physiological reports · 2023Article
- Roxadustat Attenuates the Disruption of Epithelial Tight Junction in Caco2 Cells and a Rat Model of CKD Through MicroRNA-223.Frontiers in medicine · 2022Article
- Nitric Oxide and Hydrogen Sulfide Regulation of Ischemic Vascular Growth and Remodeling.Comprehensive Physiology · 2019Review
- Restoration of skeletal muscle homeostasis by hydrogen sulfide during hyperhomocysteinemia-mediated oxidative/ER stress conditionCanadian journal of physiology and pharmacology · 2019Review
- Hydrogen sulfide alleviates hyperhomocysteinemia-mediated skeletal muscle atrophy via mitigation of oxidative and endoplasmic reticulum stress injury.American journal of physiology. Cell physiology · 2018Article
- Hydrogen sulfide improves postischemic neoangiogenesis in the hind limb of cystathionine-β-synthase mutant mice via PPAR-γ/VEGF axis.Physiological reports · 2018Article
- Exercise mitigates the effects of hyperhomocysteinemia on adverse muscle remodeling.Physiological reports · 2018Article
- Cardiac myocyte p38α kinase regulates angiogenesis via myocyte-endothelial cell cross-talk during stress-induced remodeling in the heart.The Journal of biological chemistry · 2017Article
- Mdivi-1 induced acute changes in the angiogenic profile after ischemia-reperfusion injury in female mice.Physiological reports · 2017Article
- Nitrite Prevents Right Ventricular Failure and Remodeling Induced by Pulmonary Artery Banding.Journal of cardiovascular pharmacology · 2017Article
- Hyperhomocysteinemia inhibits satellite cell regenerative capacity through p38 alpha/beta MAPK signaling.American journal of physiology. Heart and circulatory physiology · 2015Article
- Hyperhomocysteinemia associated skeletal muscle weakness involves mitochondrial dysfunction and epigenetic modifications.Biochimica et biophysica acta · 2015Article
- Mechanisms of hyperhomocysteinemia induced skeletal muscle myopathy after ischemia in the CBS-/+ mouse model.International journal of molecular sciences · 2015Article
- Role of mitochondrial fission and fusion in cardiomyocyte contractility.International journal of cardiology · 2015Article
- Modulation of hydrogen sulfide by vascular hypoxia.Hypoxia (Auckland, N.Z.) · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hyperhomocysteinemia (HHcy) is associated with elderly frailty, skeletal muscle injury and malfunction, reduced vascular integrity and function, and mortality. Although HHcy has been implicated in the impairment of angiogenesis after hindlimb ischemia in murine models, the underlying mechanisms are still unclear. We hypothesized that HHcy compromises skeletal muscle perfusion, collateral formation, and arteriogenesis by diminishing postischemic vasculogenic responses in muscle fibers. To test this hypothesis, we created femoral artery ligation in wild-type and heterozygous cystathionine β-synthase (CBS(+/-)) mice (a model for HHcy) and assessed tissue perfusion, collateral vessel formation, and skeletal muscle function using laser-Doppler perfusion imaging, barium angiography, and fatigue tests. In addition, we assessed postischemic levels of VEGF and levels of its muscle-specific regulators: hypoxia-inducible factor (HIF)-1α and peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α. The observations indicated dysregulation of VEGF, HIF-1α, and PGC-1α levels in ischemic skeletal muscles of CBS(+/-) mice. Concomitant with the reduced ischemic angiogenic responses, we also observed diminished leptin expression and attenuated Akt signaling in ischemic muscle fibers of CBS(+/-) mice. Moreover, there was enhanced atrogene, ubiquitin ligases that conjugate proteins for degradation during muscle atrophy, transcription, and reduced muscle function after ischemia in CBS(+/-) mice. These results suggest that HHcy adversely affects muscle-specific ischemic responses and contributes to muscle frailty.
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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.