{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T12:06:13Z","timestamp":1791633973284,"version":"4.3.4"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,3,17]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Clinical trials have indicated that finerenone, a nonsteroidal mineralocorticoid receptor antagonist, elicits considerable cardiovascular protective benefits; however, its precise mechanism of action remains to be fully elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">Here, we examined the impact of finerenone on myocardial injury and sodium accumulation in uninephrectomy male Sprague\u2010Dawley rats subjected to chronic aldosterone infusion (0.75\u2009\u03bcg\/h) and salt\u2010loading (1% NaCl) in drinking water for 4\u2009weeks.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">Echocardiographic assessments and gene expression analyses revealed adverse cardiac remodeling and ventricular dysfunction with preserved ejection fraction in aldosterone\/salt\u2010loaded uninephrectomy rats. Notably, finerenone (10\u2009mg\/kg) treatment completely prevented the development of cardiac dysfunction in these animals. Additionally, sodium content in left ventricular tissues was markedly elevated in aldosterone\/salt\u2010loaded uninephrectomy rats, which was attenuated by finerenone treatment. Furthermore, a significant increase in macrophage recruitment was observed in cardiac tissues with markedly elevated M1 macrophage populations. However, finerenone treatment effectively prevented migration as well as polarization of macrophage in cardiac tissue. In an in\u00a0vitro assay using RAW264.7 cells, a macrophage cell line, finerenone dramatically reduced the aldosterone\/salt\u2010induced elevation of M1 markers, whereas M2 markers exhibited a tendency to increase, potentially linked to NFAT5 (nuclear factor of activated T\u2010cells 5)\u2010 and IL (interleukin)\u201010\u2010mediated pathways.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">These findings suggest that finerenone inhibits cardiac dysfunction induced by aldosterone\/salt through the suppression of sodium accumulation in left ventricular tissues and attenuate subsequent macrophage\u2010mediated inflammation, thereby preventing adverse cardiac remodeling and dysfunction.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.044798","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T12:43:59Z","timestamp":1772628239000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["Cardioprotective Effects of Finerenone Associated With the Suppression of Myocardial Sodium Accumulation in Aldosterone\/Salt\u2010Loaded Rats"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9172-5343","authenticated-orcid":false,"given":"Asadur","family":"Rahman","sequence":"first","affiliation":[{"name":"Kagawa University","place":["Takamatsu, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1713-2045","authenticated-orcid":false,"given":"Tatsuya","family":"Sawano","sequence":"additional","affiliation":[{"name":"Tottori University","place":["Yonago, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6738-1253","authenticated-orcid":false,"given":"Kento","family":"Kitada","sequence":"additional","affiliation":[{"name":"Kagawa University","place":["Takamatsu, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-5258-5972","authenticated-orcid":false,"given":"Nourin","family":"Jahan","sequence":"additional","affiliation":[{"name":"Kagawa University","place":["Takamatsu, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihide","family":"Fujisawa","sequence":"additional","affiliation":[{"name":"Kagawa University","place":["Takamatsu, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiko","family":"Yamakawa","sequence":"additional","affiliation":[{"name":"Kagawa University","place":["Takamatsu, 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