{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T09:19:29Z","timestamp":1789982369858,"version":"4.0.1"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2012,7,24]]},"abstract":"<jats:sec>\n                    <jats:title>Background\u2014<\/jats:title>\n                    <jats:p>Inflammation plays a critical role in adverse cardiac remodeling and heart failure. Therefore, approaches geared toward inhibiting inflammation may provide therapeutic benefits. We tested the hypotheses that genetic deletion of interleukin-10 (IL-10), a potent antiinflammatory cytokine, exacerbates pressure overload\u2013induced adverse cardiac remodeling and hypertrophy and that IL-10 therapy inhibits this pathology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and Results\u2014<\/jats:title>\n                    <jats:p>Cardiac hypertrophy was induced in wild-type and IL-10 knockout mice by isoproterenol (ISO) infusion. ISO-induced left ventricular dysfunction and hypertrophic remodeling, including fibrosis and fetal gene expression, were further exaggerated in knockout mice compared with wild-type mice. Systemic recombinant mouse IL-10 administration markedly improved left ventricular function and not only inhibited but also reversed ISO-induced cardiac remodeling. Intriguingly, a very similar cardioprotective response of IL-10 was found in transverse aortic constriction\u2013induced hypertrophy and heart failure models. In neonatal rat ventricular myocytes and H9c2 myoblasts, ISO activated nuclear factor-\u03baB and inhibited signal transducers and activators of transcription 3 (STAT3) phosphorylation. Interestingly, IL-10 suppressed ISO-induced nuclear factor-\u03baB activation and attenuated STAT3 inhibition. Moreover, pharmacological and genetic inhibition of STAT3 reversed the protective effects of IL-10, whereas ectopic expression of constitutively active STAT3 mimicked the IL-10 responses on the ISO effects, confirming that the IL-10\u2013mediated inhibition of nuclear factor-\u03baB is STAT3 dependent.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion\u2014<\/jats:title>\n                    <jats:p>Taken together, our results suggest IL-10 treatment as a potential therapeutic approach to limit the progression of pressure overload\u2013induced adverse cardiac remodeling.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.112.112185","type":"journal-article","created":{"date-parts":[[2012,6,17]],"date-time":"2012-06-17T17:22:09Z","timestamp":1339953729000},"page":"418-429","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":194,"title":["Interleukin-10 Treatment Attenuates Pressure Overload\u2013Induced Hypertrophic Remodeling and Improves Heart Function via Signal Transducers and Activators of Transcription 3\u2013Dependent Inhibition of Nuclear Factor-\u03baB"],"prefix":"10.1161","volume":"126","author":[{"given":"Suresh Kumar","family":"Verma","sequence":"first","affiliation":[{"name":"From the Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL (S.K.V., P.K., N.S., R.G., E.L., M.T., A.M., E.H., V.R., G.Q., A.K.G., R.K.), and Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (D.B., S.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prasanna","family":"Krishnamurthy","sequence":"additional","affiliation":[{"name":"From the Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL (S.K.V., P.K., N.S., R.G., E.L., M.T., A.M., E.H., V.R., G.Q., A.K.G., R.K.), and Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (D.B., S.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Barefield","sequence":"additional","affiliation":[{"name":"From the Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL (S.K.V., P.K., N.S., R.G., E.L., M.T., A.M., E.H., V.R., G.Q., A.K.G., R.K.), and Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (D.B., S.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neha","family":"Singh","sequence":"additional","affiliation":[{"name":"From the Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL (S.K.V., P.K., N.S., R.G., E.L., M.T., A.M., E.H., V.R., G.Q., A.K.G., R.K.), and Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (D.B., S.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajesh","family":"Gupta","sequence":"additional","affiliation":[{"name":"From the Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL (S.K.V., P.K., N.S., R.G., E.L., M.T., A.M., E.H., V.R., G.Q., A.K.G., R.K.), and Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (D.B., 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