{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:39:22Z","timestamp":1772159962346,"version":"3.50.1"},"reference-count":27,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2020,8,2]],"date-time":"2020-08-02T00:00:00Z","timestamp":1596326400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hypoxia induces cell injury in cardiomyocytes and leads to the development of cardiovascular diseases. The survival motor neuron protein (SMN) is a crucial ubiquitous protein whose functional deficiency causes motor neuron loss seen in spinal muscular atrophy. SMN has shown protective effects on the cardiovascular system and the aim of the present study was to investigate the cardioprotective effects of SMN on hypoxia\u2010induced cell injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Cobalt chloride (CoCl\n                      <jats:sub>2<\/jats:sub>\n                      ) was used to induce chemical hypoxia in H9c2 cardiomyocytes. Cell proliferation was determined by the MTT assay and the mRNA levels of SMN were evaluated by real\u2010time polymerase chain reaction. The protein expression levels of SMN, hypoxia\u2010inducible transcription factor 1\u03b1 (HIF\u20101\u03b1), and apoptosis\u2010related proteins, such as cytochrome c (Cyt c), B cell lymphoma\u20102 (Bcl\u20102), Bcl\u20102 associated X protein (Bax), and cleaved caspase\u20103 were evaluated by western blot analysis. Cell apoptosis was analysed using annexin V\/propidium iodide (PI) staining.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Treatment with CoCl\n                      <jats:sub>2<\/jats:sub>\n                      significantly reduced H9c2 cell viability; the level of HIF\u20101\u03b1, which is a hypoxia\u2010related indicator increased whereas the expression of SMN protein decreased. Hypoxia also induced cardiomyocyte apoptosis, indicated by reduced Bcl\u20102 expression and elevated cleaved caspase\u20103, Bax, and cytochrome c levels. Interestingly, SMN, which is a neuron protection factor, ameliorated CoCl\n                      <jats:sub>2<\/jats:sub>\n                      \u2010induced cell damage by reducing cardiomyocyte apoptosis through upregulation of Bcl\u20102 and inhibition of cytochrome c, cleaved caspase\u20103, and Bax expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Survival motor neuron prevents hypoxia\u2010induced cell apoptosis through inhibition of the mitochondrial apoptotic pathway, and thereby exerts a protective effect on H9c2 cardiomyocytes.<\/jats:p>\n                  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