Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice
Objective This study investigated whether levels of signaling pathways and inflammatory adipokines in epicardial fat regulate cardiovascular risks in humans and mice. Methods Epicardial fat was obtained from the hearts of patients with heart failure requiring coronary artery bypass surgery, and sign...
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| Veröffentlicht in: | Obesity (Silver Spring, Md.) Md.), 2019-10, Vol.27 (10), p.1634-1643 |
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| container_title | Obesity (Silver Spring, Md.) |
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| creator | Singh, Shailendra P. McClung, John A. Thompson, Ellen Glick, Yosef Greenberg, Menachem Acosta‐Baez, Giancarlo Edris, Basel Shapiro, Joseph I. Abraham, Nader G. |
| description | Objective
This study investigated whether levels of signaling pathways and inflammatory adipokines in epicardial fat regulate cardiovascular risks in humans and mice.
Methods
Epicardial fat was obtained from the hearts of patients with heart failure requiring coronary artery bypass surgery, and signaling pathways were compared with visceral fat. The genetic profile of epicardial and visceral fat from humans was also compared with genetic profiles of epicardial and visceral fat in obese mice. Left ventricular (LV) fractional shortening was measured in obese mice before and after treatment with inducers of mitochondrial signaling heme oxygenase 1 (HO‐1)‐peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α). An RNA array/heat map on 88 genes that regulate adipose tissue function was used to identify a target gene network.
Results
Human epicardial fat gene profiling showed decreased levels of mitochondrial signaling of HO‐1‐PGC1α and increased levels of the inflammatory adipokine CCN family member 3. Similar observations were seen in epicardial and visceral fat of obese mice. Improvement in LV function was linked to the increase in mitochondrial signaling in epicardial fat of obese mice.
Conclusions
There is a link between cardiac ectopic fat deposition and cardiac function in humans that is similar to that which is described in obese mice. An increase of mitochondrial signaling pathway gene expression in epicardial fat attenuates cardiometabolic dysfunction and LV fractional shortening in obese mice. |
| doi_str_mv | 10.1002/oby.22608 |
| format | Article |
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This study investigated whether levels of signaling pathways and inflammatory adipokines in epicardial fat regulate cardiovascular risks in humans and mice.
Methods
Epicardial fat was obtained from the hearts of patients with heart failure requiring coronary artery bypass surgery, and signaling pathways were compared with visceral fat. The genetic profile of epicardial and visceral fat from humans was also compared with genetic profiles of epicardial and visceral fat in obese mice. Left ventricular (LV) fractional shortening was measured in obese mice before and after treatment with inducers of mitochondrial signaling heme oxygenase 1 (HO‐1)‐peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α). An RNA array/heat map on 88 genes that regulate adipose tissue function was used to identify a target gene network.
Results
Human epicardial fat gene profiling showed decreased levels of mitochondrial signaling of HO‐1‐PGC1α and increased levels of the inflammatory adipokine CCN family member 3. Similar observations were seen in epicardial and visceral fat of obese mice. Improvement in LV function was linked to the increase in mitochondrial signaling in epicardial fat of obese mice.
Conclusions
There is a link between cardiac ectopic fat deposition and cardiac function in humans that is similar to that which is described in obese mice. An increase of mitochondrial signaling pathway gene expression in epicardial fat attenuates cardiometabolic dysfunction and LV fractional shortening in obese mice.</description><identifier>ISSN: 1930-7381</identifier><identifier>EISSN: 1930-739X</identifier><identifier>DOI: 10.1002/oby.22608</identifier><identifier>PMID: 31441604</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adipocytes ; Adipose Tissue - metabolism ; Aged ; Animals ; Biosynthesis ; Bone marrow ; Carbon monoxide ; Cardiovascular Diseases - genetics ; Cardiovascular Diseases - metabolism ; Cardiovascular Diseases - physiopathology ; Cell adhesion & migration ; Coronary vessels ; Cytokines ; Cytoprotection - genetics ; Diabetes ; Female ; Gene expression ; Heart failure ; Heart surgery ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Humans ; Hypertension ; Insulin resistance ; Intra-Abdominal Fat - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Middle Aged ; Myocardium - metabolism ; Myocardium - pathology ; Obesity ; Obesity - complications ; Obesity - genetics ; Obesity - metabolism ; Original ; Oxidative stress ; Pericardium - metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; Proteins ; Risk Factors ; Signal Transduction - physiology</subject><ispartof>Obesity (Silver Spring, Md.), 2019-10, Vol.27 (10), p.1634-1643</ispartof><rights>2019 The Authors. Obesity published by Wiley Periodicals, Inc. on behalf of The Obesity Society (TOS)</rights><rights>2019 The Authors. Obesity published by Wiley Periodicals, Inc. on behalf of The Obesity Society (TOS).</rights><rights>Copyright Blackwell Publishing Ltd. Oct 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4438-e84bd20248f023645fb770616ed746caf8801c0fcc2fc6cc4d5d80c1b57199df3</citedby><cites>FETCH-LOGICAL-c4438-e84bd20248f023645fb770616ed746caf8801c0fcc2fc6cc4d5d80c1b57199df3</cites><orcidid>0000-0001-8983-1959</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Foby.22608$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Foby.22608$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31441604$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Singh, Shailendra P.</creatorcontrib><creatorcontrib>McClung, John A.</creatorcontrib><creatorcontrib>Thompson, Ellen</creatorcontrib><creatorcontrib>Glick, Yosef</creatorcontrib><creatorcontrib>Greenberg, Menachem</creatorcontrib><creatorcontrib>Acosta‐Baez, Giancarlo</creatorcontrib><creatorcontrib>Edris, Basel</creatorcontrib><creatorcontrib>Shapiro, Joseph I.</creatorcontrib><creatorcontrib>Abraham, Nader G.</creatorcontrib><title>Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice</title><title>Obesity (Silver Spring, Md.)</title><addtitle>Obesity (Silver Spring)</addtitle><description>Objective
This study investigated whether levels of signaling pathways and inflammatory adipokines in epicardial fat regulate cardiovascular risks in humans and mice.
Methods
Epicardial fat was obtained from the hearts of patients with heart failure requiring coronary artery bypass surgery, and signaling pathways were compared with visceral fat. The genetic profile of epicardial and visceral fat from humans was also compared with genetic profiles of epicardial and visceral fat in obese mice. Left ventricular (LV) fractional shortening was measured in obese mice before and after treatment with inducers of mitochondrial signaling heme oxygenase 1 (HO‐1)‐peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α). An RNA array/heat map on 88 genes that regulate adipose tissue function was used to identify a target gene network.
Results
Human epicardial fat gene profiling showed decreased levels of mitochondrial signaling of HO‐1‐PGC1α and increased levels of the inflammatory adipokine CCN family member 3. Similar observations were seen in epicardial and visceral fat of obese mice. Improvement in LV function was linked to the increase in mitochondrial signaling in epicardial fat of obese mice.
Conclusions
There is a link between cardiac ectopic fat deposition and cardiac function in humans that is similar to that which is described in obese mice. An increase of mitochondrial signaling pathway gene expression in epicardial fat attenuates cardiometabolic dysfunction and LV fractional shortening in obese mice.</description><subject>Adipocytes</subject><subject>Adipose Tissue - metabolism</subject><subject>Aged</subject><subject>Animals</subject><subject>Biosynthesis</subject><subject>Bone marrow</subject><subject>Carbon monoxide</subject><subject>Cardiovascular Diseases - genetics</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cardiovascular Diseases - physiopathology</subject><subject>Cell adhesion & migration</subject><subject>Coronary vessels</subject><subject>Cytokines</subject><subject>Cytoprotection - genetics</subject><subject>Diabetes</subject><subject>Female</subject><subject>Gene expression</subject><subject>Heart failure</subject><subject>Heart surgery</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Insulin resistance</subject><subject>Intra-Abdominal Fat - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Obese</subject><subject>Middle Aged</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Pericardium - metabolism</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</subject><subject>Proteins</subject><subject>Risk Factors</subject><subject>Signal Transduction - physiology</subject><issn>1930-7381</issn><issn>1930-739X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp1kU9u1DAUhy0EoqWw4ALIEhtYTGs7juNskMqo7SAVDeKPBCvLcV4Gl8Se2snA7BAn4CpcpIfoSXBIGQESC8t-8vc-Pb0fQg8pOaSEsCNfbQ8ZE0TeQvu0zMisyMr3t3dvSffQvRgvCOGC5PQu2sso51QQvo--zXWorV8H34Pp7QbwAjrAyy_bFTgd4frrd5rOq7M5vfqB39iV0611K2wdPllbMzbrFp_qHh_3PbhB9xDx5NzoaIZWB_zaxk9jw2LotItYx7FYVhABv7QG7qM7jW4jPLi5D9C705O388XsfHn2Yn58PjOcZ3IGklc1I4zLhrBM8LypioIIKqAuuDC6kZJQQxpjWGOEMbzOa0kMrfKClmXdZAfo2eRdD1UHtQHXB92qdbCdDlvltVV__zj7Ua38RokiFyXPk-DJjSD4ywFirzobDbStduCHqBiTMm2eS5rQx_-gF34IaXcjVcqC5TRniXo6USb4GAM0u2EoUWOyKiWrfiWb2Ed_Tr8jf0eZgKMJ-Gxb2P7fpJbPP0zKn8ERsR8</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Singh, Shailendra P.</creator><creator>McClung, John A.</creator><creator>Thompson, Ellen</creator><creator>Glick, Yosef</creator><creator>Greenberg, Menachem</creator><creator>Acosta‐Baez, Giancarlo</creator><creator>Edris, Basel</creator><creator>Shapiro, Joseph I.</creator><creator>Abraham, Nader G.</creator><general>Blackwell Publishing Ltd</general><general>John Wiley and Sons Inc</general><scope>24P</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>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8983-1959</orcidid></search><sort><creationdate>201910</creationdate><title>Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice</title><author>Singh, Shailendra P. ; McClung, John A. ; Thompson, Ellen ; Glick, Yosef ; Greenberg, Menachem ; Acosta‐Baez, Giancarlo ; Edris, Basel ; Shapiro, Joseph I. ; Abraham, Nader G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4438-e84bd20248f023645fb770616ed746caf8801c0fcc2fc6cc4d5d80c1b57199df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adipocytes</topic><topic>Adipose Tissue - metabolism</topic><topic>Aged</topic><topic>Animals</topic><topic>Biosynthesis</topic><topic>Bone marrow</topic><topic>Carbon monoxide</topic><topic>Cardiovascular Diseases - genetics</topic><topic>Cardiovascular Diseases - metabolism</topic><topic>Cardiovascular Diseases - physiopathology</topic><topic>Cell adhesion & migration</topic><topic>Coronary vessels</topic><topic>Cytokines</topic><topic>Cytoprotection - genetics</topic><topic>Diabetes</topic><topic>Female</topic><topic>Gene expression</topic><topic>Heart failure</topic><topic>Heart surgery</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Insulin resistance</topic><topic>Intra-Abdominal Fat - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Obese</topic><topic>Middle Aged</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Pericardium - metabolism</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</topic><topic>Proteins</topic><topic>Risk Factors</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Singh, Shailendra P.</creatorcontrib><creatorcontrib>McClung, John A.</creatorcontrib><creatorcontrib>Thompson, Ellen</creatorcontrib><creatorcontrib>Glick, Yosef</creatorcontrib><creatorcontrib>Greenberg, Menachem</creatorcontrib><creatorcontrib>Acosta‐Baez, Giancarlo</creatorcontrib><creatorcontrib>Edris, Basel</creatorcontrib><creatorcontrib>Shapiro, Joseph I.</creatorcontrib><creatorcontrib>Abraham, Nader G.</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Obesity (Silver Spring, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Singh, Shailendra P.</au><au>McClung, John A.</au><au>Thompson, Ellen</au><au>Glick, Yosef</au><au>Greenberg, Menachem</au><au>Acosta‐Baez, Giancarlo</au><au>Edris, Basel</au><au>Shapiro, Joseph I.</au><au>Abraham, Nader G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice</atitle><jtitle>Obesity (Silver Spring, Md.)</jtitle><addtitle>Obesity (Silver Spring)</addtitle><date>2019-10</date><risdate>2019</risdate><volume>27</volume><issue>10</issue><spage>1634</spage><epage>1643</epage><pages>1634-1643</pages><issn>1930-7381</issn><eissn>1930-739X</eissn><abstract>Objective
This study investigated whether levels of signaling pathways and inflammatory adipokines in epicardial fat regulate cardiovascular risks in humans and mice.
Methods
Epicardial fat was obtained from the hearts of patients with heart failure requiring coronary artery bypass surgery, and signaling pathways were compared with visceral fat. The genetic profile of epicardial and visceral fat from humans was also compared with genetic profiles of epicardial and visceral fat in obese mice. Left ventricular (LV) fractional shortening was measured in obese mice before and after treatment with inducers of mitochondrial signaling heme oxygenase 1 (HO‐1)‐peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α). An RNA array/heat map on 88 genes that regulate adipose tissue function was used to identify a target gene network.
Results
Human epicardial fat gene profiling showed decreased levels of mitochondrial signaling of HO‐1‐PGC1α and increased levels of the inflammatory adipokine CCN family member 3. Similar observations were seen in epicardial and visceral fat of obese mice. Improvement in LV function was linked to the increase in mitochondrial signaling in epicardial fat of obese mice.
Conclusions
There is a link between cardiac ectopic fat deposition and cardiac function in humans that is similar to that which is described in obese mice. An increase of mitochondrial signaling pathway gene expression in epicardial fat attenuates cardiometabolic dysfunction and LV fractional shortening in obese mice.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>31441604</pmid><doi>10.1002/oby.22608</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-8983-1959</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipose Tissue - metabolism Aged Animals Biosynthesis Bone marrow Carbon monoxide Cardiovascular Diseases - genetics Cardiovascular Diseases - metabolism Cardiovascular Diseases - physiopathology Cell adhesion & migration Coronary vessels Cytokines Cytoprotection - genetics Diabetes Female Gene expression Heart failure Heart surgery Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism Humans Hypertension Insulin resistance Intra-Abdominal Fat - metabolism Male Mice Mice, Inbred C57BL Mice, Obese Middle Aged Myocardium - metabolism Myocardium - pathology Obesity Obesity - complications Obesity - genetics Obesity - metabolism Original Oxidative stress Pericardium - metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Proteins Risk Factors Signal Transduction - physiology |
| title | Cardioprotective Heme Oxygenase‐1‐PGC1α Signaling in Epicardial Fat Attenuates Cardiovascular Risk in Humans as in Obese Mice |
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