Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease
Peripheral arterial disease (PAD) is associated with an increased risk of overall cardiovascular mortality, and substantial morbidity resulting from claudication. While the initial disease process is clearly the result of atherosclerosis in the arterial circulation of the limb, altered hemodynamics...
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Veröffentlicht in: | Vascular medicine (London, England) England), 2000-02, Vol.5 (1), p.55-59 |
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description | Peripheral arterial disease (PAD) is associated with an increased risk of overall cardiovascular mortality, and substantial morbidity resulting from claudication. While the initial disease process is clearly the result of atherosclerosis in the arterial circulation of the limb, altered hemodynamics do not completely explain the pathophysiology of claudication. Work from several laboratories has demonstrated secondary changes in the skeletal muscle of patients with PAD which are consistent with the presence of an acquired metabolic myopathy in these patients. Key findings include an alteration in the expression of mitochondrial enzymes, the accumulation of metabolic intermediates, altered regulation of mitochondrial respiration, increased oxidative stress, and the presence of somatic mutations in the mitochondrial genome. Understanding the metabolic changes associated with PAD is important in understanding the pathophysiology of claudication and in the development of novel therapeutic strategies. |
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While the initial disease process is clearly the result of atherosclerosis in the arterial circulation of the limb, altered hemodynamics do not completely explain the pathophysiology of claudication. Work from several laboratories has demonstrated secondary changes in the skeletal muscle of patients with PAD which are consistent with the presence of an acquired metabolic myopathy in these patients. Key findings include an alteration in the expression of mitochondrial enzymes, the accumulation of metabolic intermediates, altered regulation of mitochondrial respiration, increased oxidative stress, and the presence of somatic mutations in the mitochondrial genome. 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Miscellaneous ; DNA, Mitochondrial - genetics ; Humans ; Medical sciences ; Mitochondria, Muscle - enzymology ; Mitochondria, Muscle - genetics ; Muscle, Skeletal - metabolism ; Muscular Diseases - etiology ; Muscular Diseases - metabolism ; Mutation ; Peripheral Vascular Diseases - complications ; Peripheral Vascular Diseases - metabolism</subject><ispartof>Vascular medicine (London, England), 2000-02, Vol.5 (1), p.55-59</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-7580e75c291b88a13fa2a93ab27190b18c5b4a522c7baedf2987044ae1b10afc3</citedby><cites>FETCH-LOGICAL-c434t-7580e75c291b88a13fa2a93ab27190b18c5b4a522c7baedf2987044ae1b10afc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/1358836X0000500109$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/1358836X0000500109$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21819,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1277242$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10737157$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brass, Eric P</creatorcontrib><creatorcontrib>Hiatt, William R</creatorcontrib><title>Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease</title><title>Vascular medicine (London, England)</title><addtitle>Vasc Med</addtitle><description>Peripheral arterial disease (PAD) is associated with an increased risk of overall cardiovascular mortality, and substantial morbidity resulting from claudication. While the initial disease process is clearly the result of atherosclerosis in the arterial circulation of the limb, altered hemodynamics do not completely explain the pathophysiology of claudication. Work from several laboratories has demonstrated secondary changes in the skeletal muscle of patients with PAD which are consistent with the presence of an acquired metabolic myopathy in these patients. Key findings include an alteration in the expression of mitochondrial enzymes, the accumulation of metabolic intermediates, altered regulation of mitochondrial respiration, increased oxidative stress, and the presence of somatic mutations in the mitochondrial genome. Understanding the metabolic changes associated with PAD is important in understanding the pathophysiology of claudication and in the development of novel therapeutic strategies.</description><subject>Animals</subject><subject>Arteriosclerosis - complications</subject><subject>Arteriosclerosis - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>DNA, Mitochondrial - genetics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mitochondria, Muscle - enzymology</subject><subject>Mitochondria, Muscle - genetics</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscular Diseases - etiology</subject><subject>Muscular Diseases - metabolism</subject><subject>Mutation</subject><subject>Peripheral Vascular Diseases - complications</subject><subject>Peripheral Vascular Diseases - metabolism</subject><issn>1358-836X</issn><issn>1358-863X</issn><issn>1477-0377</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1Lw0AQhhdRbK3-AQ-Sg3iL3dkkneRYil9Q8KIgXsJkM9HUpEl3k0P_vRtSUBCcy8zsPO8M-wpxCfIWAHEOQRTHweJNuoikBJkciSmEiL4MEI9d7QB_ICbizNqNw3CRwKmYgMQAIcKpeF_qXV8azj37xRV3VHl1b3XFXu2arKlK7dX7pqXuc--VW89lNs0AmKZzs5ZN2bonpyPTucYVeWmZLJ-Lk4IqyxeHPBOv93cvq0d__fzwtFqufR0GYedjFEvGSKsEsjgmCApSlASUKYREZhDrKAspUkpjRpwXKolRhiExZCCp0MFM3Ix7W9PserZdWpdWc1XRlpvepgiDP6AcqEZQux9Yw0XamrIms09BpoOj6V9HnejqsL3Pas5_SUYLHXB9AMhqqgpDW13aH04hqnA4Ph8xSx-cbprebJ0p_13-BkeVjJg</recordid><startdate>20000201</startdate><enddate>20000201</enddate><creator>Brass, Eric P</creator><creator>Hiatt, William R</creator><general>Sage Publications</general><general>Arnold</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20000201</creationdate><title>Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease</title><author>Brass, Eric P ; Hiatt, William R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-7580e75c291b88a13fa2a93ab27190b18c5b4a522c7baedf2987044ae1b10afc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Arteriosclerosis - complications</topic><topic>Arteriosclerosis - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>DNA, Mitochondrial - genetics</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mitochondria, Muscle - enzymology</topic><topic>Mitochondria, Muscle - genetics</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscular Diseases - etiology</topic><topic>Muscular Diseases - metabolism</topic><topic>Mutation</topic><topic>Peripheral Vascular Diseases - complications</topic><topic>Peripheral Vascular Diseases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brass, Eric P</creatorcontrib><creatorcontrib>Hiatt, William R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Vascular medicine (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brass, Eric P</au><au>Hiatt, William R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease</atitle><jtitle>Vascular medicine (London, England)</jtitle><addtitle>Vasc Med</addtitle><date>2000-02-01</date><risdate>2000</risdate><volume>5</volume><issue>1</issue><spage>55</spage><epage>59</epage><pages>55-59</pages><issn>1358-836X</issn><issn>1358-863X</issn><eissn>1477-0377</eissn><abstract>Peripheral arterial disease (PAD) is associated with an increased risk of overall cardiovascular mortality, and substantial morbidity resulting from claudication. While the initial disease process is clearly the result of atherosclerosis in the arterial circulation of the limb, altered hemodynamics do not completely explain the pathophysiology of claudication. Work from several laboratories has demonstrated secondary changes in the skeletal muscle of patients with PAD which are consistent with the presence of an acquired metabolic myopathy in these patients. Key findings include an alteration in the expression of mitochondrial enzymes, the accumulation of metabolic intermediates, altered regulation of mitochondrial respiration, increased oxidative stress, and the presence of somatic mutations in the mitochondrial genome. Understanding the metabolic changes associated with PAD is important in understanding the pathophysiology of claudication and in the development of novel therapeutic strategies.</abstract><cop>Thousand Oaks, CA</cop><pub>Sage Publications</pub><pmid>10737157</pmid><doi>10.1177/1358836X0000500109</doi><tpages>5</tpages></addata></record> |
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subjects | Animals Arteriosclerosis - complications Arteriosclerosis - metabolism Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous DNA, Mitochondrial - genetics Humans Medical sciences Mitochondria, Muscle - enzymology Mitochondria, Muscle - genetics Muscle, Skeletal - metabolism Muscular Diseases - etiology Muscular Diseases - metabolism Mutation Peripheral Vascular Diseases - complications Peripheral Vascular Diseases - metabolism |
title | Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease |
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