{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:31:38Z","timestamp":1792787498562,"version":"4.5.0"},"reference-count":32,"publisher":"American Physiological Society","issue":"5","funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft (DFG)","doi-asserted-by":"publisher","award":["SFB 688"],"award-info":[{"award-number":["SFB 688"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft (DFG)","doi-asserted-by":"publisher","award":["TPA10"],"award-info":[{"award-number":["TPA10"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft (DFG)","doi-asserted-by":"publisher","award":["RA2824\/1-1"],"award-info":[{"award-number":["RA2824\/1-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Interdisciplinary Center foe Clinical Research (W\u00fcrzburg)","award":["E-354"],"award-info":[{"award-number":["E-354"]}]},{"name":"Graduate School of Life Sciences"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2018,11,1]]},"abstract":"<jats:p>\n                    Heart-specific antibodies have been widely associated with myocardial infarction (MI). However, it remains unclear whether autoantibodies mediate disease progression or are a byproduct of cardiac injury. To disambiguate the role of immunoglobulins in MI, we characterized the development of ischemic heart failure in agammaglobulinemic mice (AID\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    \u03bcS\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ). Although these animals can produce functional B cells, they cannot synthesize secretory IgM (\u03bcS\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) or perform Ig class switching (AID\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ), leading to complete antibody deficiency. Agammaglobulinemia did not affect overall post-MI survival but resulted in a significant reduction in infarct size. Echocardiographic analyses showed that, compared with wild-type infarcted control mice, AID\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    \u03bcS\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice exhibited improved cardiac function and reduced remodeling on day 56 post-MI. These differences remained significant even after animals with matched infarct sizes were compared. Infarcted AID\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    \u03bcS\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice also showed reduced myocardial expression levels of transcripts known to promote adverse remodeling, such as matrix metalloproteinase-9, collagen type I a1, collagen type III a1, and IL-6. An unbiased screening of the heart reactivity potential in the plasma of wild-type MI animals revealed the presence of antibodies that target the myocardial scar and collagenase-sensitive epitopes. Moreover, we found that IgG accumulated within the scar tissues of infarcted mice and remained in close proximity with cells expressing Fc\u03b3 receptors (CD16\/32), suggesting the existence of an in situ IgG-Fc\u03b3 receptor axis. Collectively, our study results confirm that antibodies contribute to ischemic heart failure progression and provide novel insights into the mechanisms underlying this phenomenon.\n                  <\/jats:p>\n                  <jats:p>NEW &amp; NOTEWORTHY Our study sheds some light on the long-standing debate over the relevance of autoantibodies in heart failure and might stimulate future research in the field. The observation of extracellular matrix-specific antibodies and the detection of Fc\u03b3 receptor-expressing cells within the scar provide novel insights into the mechanisms by which antibodies may contribute to adverse remodeling.<\/jats:p>","DOI":"10.1152\/ajpheart.00144.2018","type":"journal-article","created":{"date-parts":[[2018,8,10]],"date-time":"2018-08-10T14:35:05Z","timestamp":1533911705000},"page":"H1358-H1367","source":"Crossref","is-referenced-by-count":36,"title":["Antibodies aggravate the development of ischemic heart failure"],"prefix":"10.1152","volume":"315","author":[{"given":"Lea","family":"Keppner","sequence":"first","affiliation":[{"name":"University Hospital Halle, Department of Internal Medicine-III, Halle, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margarete","family":"Heinrichs","sequence":"additional","affiliation":[{"name":"University Hospital W\u00fcrzburg, Department of Internal Medicine-I, W\u00fcrzburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Max","family":"Rieckmann","sequence":"additional","affiliation":[{"name":"University Hospital Halle, Department of Internal Medicine-III, Halle, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jocelyne","family":"Demengeot","sequence":"additional","affiliation":[{"name":"Instituto Gulbenkian de Ciencia, Oeiras, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Frantz","sequence":"additional","affiliation":[{"name":"University Hospital Halle, Department of Internal Medicine-III, Halle, Germany"},{"name":"University Hospital W\u00fcrzburg, Department of Internal Medicine-I, W\u00fcrzburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Hofmann","sequence":"additional","affiliation":[{"name":"University Hospital Halle, Department of Internal Medicine-III, Halle, Germany"},{"name":"University Hospital 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