Pathophysiology of sudden death after myocardial infarction Exploring the JAK/STAT3/SOCS3 pathway in noncardiac myocytes

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K17913
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 55060:Emergency medicine-related
• Research Institution: Kurume University
• Principal Investigator: Okabe Kouta 久留米大学, 医学部, 助教 (70840023)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 虚血性心筋症 / 急性心筋梗塞 / 致死性不整脈 / 突然死

Outline of Final Research Achievements

Smooth muscle cell-specific SOCS3-deficient mice were used for histological and molecular evaluation during acute myocardial ischemia. The results showed that although there was no significant difference in mortality at 2 weeks after myocardial infarction (MI), there were more deaths other than cardiac rupture in KOs compared to WTs. Fatal arrhythmias were identified as a cause, but no significant difference was found. Echocardiography showed a reduction in left ventricular diameter enlargement in KO compared to WT at 2 weeks post-MI, but this difference was not statistically significant.

Free Research Field

心不全、心筋症

Academic Significance and Societal Importance of the Research Achievements

急性心筋梗塞による致死性不整脈の発症は、死亡につながるだけではなく、救命後も社会復帰が困難になるなどの重症な後遺障害を生じる可能性が高い。今回、心筋以外の心臓に存在する細胞による致死性不整脈の出現の関与やメカニズムを調査することで、現在までの治療に加えた新たな治療法の開発につながることが期待された。今回の研究で致死性不整脈の出現は確認できたが、有意差は見出せなかった。しかしながら、心筋細胞以外が致死性不整脈の出現に関与している可能性を示せたと考えられる。