{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T22:58:47Z","timestamp":1784329127364,"version":"3.55.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2023,4,4]]},"abstract":"<jats:sec sec-type=\"background\" xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Pathological cardiac hypertrophy is regarded as a critical precursor and independent risk factor of heart failure, and its inhibition prevents the progression of heart failure. Switch\u2010associated protein 70 (SWAP70) is confirmed important in immunoregulation, cell maturation, and cell transformation. However, its role in pathological cardiac hypertrophy remains unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The effects of SWAP70 on pathological cardiac hypertrophy were investigated in\n              <jats:italic>Swap70<\/jats:italic>\n              knockout mice and\n              <jats:italic>Swap70<\/jats:italic>\n              overexpression\/knockdown cardiomyocytes. Bioinformatic analysis combined with multiple molecular biological methodologies were adopted to elucidate the mechanisms underlying the effects of SWAP70 on pathological cardiac hypertrophy. Results showed that SWAP70 protein levels were significantly increased in failing human heart tissues, experimental transverse aortic constriction\u2013induced mouse hypertrophic hearts, and phenylephrine\u2010stimulated isolated primary cardiomyocytes. Intriguingly, phenylephrine treatment decreased the lysosomal degradation of SWAP70 by disrupting the interaction of SWAP70 with granulin precursor. In vitro and in vivo experiments revealed that\n              <jats:italic>Swap70<\/jats:italic>\n              knockdown\/knockout accelerated the progression of pathological cardiac hypertrophy, while\n              <jats:italic>Swap70<\/jats:italic>\n              overexpression restrained the cardiomyocyte hypertrophy. SWAP70 restrained the binding of transforming growth factor \u03b2\u2010activated kinase 1 (TAK1) and TAK1 binding protein 1, thus blocking the phosphorylation of TAK1 and downstream c\u2010Jun N\u2010terminal kinase\/P38 signaling. TAK1 interacted with the N\u2010terminals (1\u2013192) of SWAP70.\n              <jats:italic>Swap70<\/jats:italic>\n              (193\u2013585) overexpression failed to inhibit cardiac hypertrophy when the TAK1\u2013SWAP70 interaction was disrupted. Either inhibiting the phosphorylation or suppressing the expression of TAK1 rescued the exaggerated cardiac hypertrophy induced by\n              <jats:italic>Swap70<\/jats:italic>\n              knockdown.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">SWAP70 suppressed the progression of cardiac hypertrophy, possibly by inhibiting the mitogen\u2010activated protein kinases signaling pathway in a TAK1\u2010dependent manner, and lysosomes are involved in the regulation of SWAP70 expression level.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.122.028628","type":"journal-article","created":{"date-parts":[[2023,3,28]],"date-time":"2023-03-28T09:20:26Z","timestamp":1679995226000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":14,"title":["SWAP70 Overexpression Protects Against Pathological 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Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dewen","family":"Leng","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Zhongnan Hospital of Wuhan University Wuhan China"},{"name":"Hubei Provincial Engineering Research Center of Minimally Invasive Cardiovascular Surgery Wuhan China"},{"name":"Wuhan Clinical Research Center for Minimally Invasive Treatment of Structural Heart Disease Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Zhongnan Hospital of Wuhan University Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongjie","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Zhongnan Hospital of Wuhan University Wuhan 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