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Impairment of NO\/soluble guanylyl cyclase (sGC)\/cGMP pathway has been reported in anthracycline\u2010induced cardiomyopathy. This raises the hypothesis that increasing cGMP by sGC stimulation could preserve cardiac function even after HF has developed. This study aimed to evaluate the long\u2010term effects of treatment with sGC stimulator BAY 41\u20108543 in a model of DOXO\u2010induced HF with nephrotic syndrome in hypertensive rats.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Male Ren\u20102 transgenic rats received five weekly intravenous injections of DOXO (cumulative dose 10\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      ) to induce cardiomyopathy. After two additional weeks, animals were treated with either BAY 41\u20108543 (10\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      \u00b7day\n                      <jats:sup>\u22121<\/jats:sup>\n                      ) or an ACE inhibitor (ACEi; trandolapril, 0.25\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      \u00b7day\n                      <jats:sup>\u22121<\/jats:sup>\n                      ). Echocardiography, blood and urine collection were performed at baseline (week \u22121) and 4\u2009weeks after the treatment started to assess cardiac ventricular function, cardiac and renal biomarkers; survival at 20\u2009weeks.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>Treatment with BAY 41\u20108543 improved long\u2010term survival, preserved left and right ventricular systolic function and reduced myocardial expression of inflammation\u2010related genes, particularly those linked to type I interferon signalling. ACEi provided stronger benefits in survival and structural remodelling. Kidney damage and function was not improved by any treatment compared to placebo.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>The sGC stimulator BAY 41\u20108543 exerted significant cardioprotective effects in DOXO\u2010induced HF. Therefore, sGC stimulators may represent a promising therapeutic option for anthracycline\u2010induced cardiomyopathy, although additional studies are required to fully investigate their therapeutic potential.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70608","type":"journal-article","created":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T02:32:37Z","timestamp":1784946757000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["sGC stimulator BAY 41\u20108543 improves survival and ventricular function in a rat model of doxorubicin\u2010induced cardiomyopathy with nephrotic syndrome"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4397-3991","authenticated-orcid":false,"given":"Olga","family":"Gawrys","sequence":"first","affiliation":[{"name":"Center for Experimental Medicine Institute for Clinical and Experimental Medicine  Prague Czech 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