ArticleArteriosclerosis, thrombosis, and vascular biology2008
Myocyte specific overexpression of myoglobin impairs angiogenesis after hind-limb ischemia.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Myoglobin-derived iron causes wound enlargement and impaired regeneration in pressure injuries of muscle.eLife · 2023Article
- Pentose Pathway Activation Is Superior to Increased Glycolysis for Therapeutic Angiogenesis in Peripheral Arterial Disease.Journal of the American Heart Association · 2023Article
- Targeting Anti-Angiogenic VEGFCells · 2022Article
- Article
- MicroRNA-30b Is Both Necessary and Sufficient for Interleukin-21 Receptor-Mediated Angiogenesis in Experimental Peripheral Arterial Disease.International journal of molecular sciences · 2021Article
- Identification of the initial molecular changes in response to circulating angiogenic cells-mediated therapy in critical limb ischemia.Stem cell research & therapy · 2020Article
- Hydrogen molecules (H2) improve perfusion recovery via antioxidant effects in experimental peripheral arterial disease.Molecular medicine reports · 2018Article
- Aerobic training and l-arginine supplementation promotes rat heart and hindleg muscles arteriogenesis after myocardial infarction.Journal of physiology and biochemistry · 2016Article
- Endothelial interleukin-21 receptor up-regulation in peripheral artery disease.Vascular medicine (London, England) · 2016Article
- ADAM12: a genetic modifier of preclinical peripheral arterial disease.American journal of physiology. Heart and circulatory physiology · 2015Article
- PADPIN: protein-protein interaction networks of angiogenesis, arteriogenesis, and inflammation in peripheral arterial disease.Physiological genomics · 2015Article
- A Pilot Study on Pain and the Upregulation of Myoglobin through Low-frequency and High-amplitude Electrical Stimulation-induced Muscle Contraction.Journal of physical therapy science · 2014Article
- Myoglobin overexpression inhibits reperfusion in the ischemic mouse hindlimb through impaired angiogenesis but not arteriogenesis.The American journal of pathology · 2013Article
- The muscle fiber type-fiber size paradox: hypertrophy or oxidative metabolism?European journal of applied physiology · 2010Review
- Myoglobin concentration in skeletal muscle fibers of chronic heart failure patients.Journal of applied physiology (Bethesda, Md. : 1985) · 2009Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveIn preclinical models of peripheral arterial disease the angiogenic response is typically robust, though it can be impaired in conditions such as hypercholesterolemia and diabetes where the endothelium is dysfunctional. Myoglobin (Mb) is expressed exclusively in striated muscle cells. We hypothesized that myocyte specific overexpression of myoglobin attenuates ischemia-induced angiogenesis even in the presence of normal endothelium. METHODS AND
resultsMb overexpressing transgenic (MbTg, n=59) and wild-type (WT, n=56) C57Bl/6 mice underwent unilateral femoral artery ligation/excision. Perfusion recovery was monitored using Laser Doppler. Ischemia-induced changes in muscle were assessed by protein and immunohistochemistry assays. Nitrite/nitrate and protein-bound NO, and vasoreactivity was measured. Vasoreactivity was similar between MbTg and WT. In ischemic muscle, at d14 postligation, MbTg increased VEGF-A, and activated eNOS the same as WT mice but nitrate/nitrite were reduced whereas protein-bound NO was higher. MbTg had attenuated perfusion recovery at d21 (0.37+/-0.03 versus 0.47+/-0.02, P<0.05), d28 (0.40+/-0.03 versus 0.50+/-0.04, P<0.05), greater limb necrosis (65.2% versus 15%, P<0.001), a lower capillary density, and greater apoptosis versus WT.
conclusionsIncreased Mb expression in myocytes attenuates angiogenesis after hind-limb ischemia by binding NO and reducing its bioavailability. Myoglobin can modulate the angiogenic response to ischemia even in the setting of normal endothelium.
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