CircRNA DICAR as a novel endogenous regulator for diabetic cardiomyopathy and diabetic pyroptosis of cardiomyocytes
作者机构：Department of Cardiologythe Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical ElectrophysiologyMinistry of EducationInstitute of Cardiovascular Research and Institute of Metabolic DiseasesSouthwest Medical UniversityLuzhou 646000China College of MedicineWuhan University of Science and TechnologyWuhan 430065China Department of Emergency and Critical Care MedicineGuangdong Provincial People’s HospitalGuangdong Academy of Medical SciencesGuangzhou 510080China China Resource&WISCO General HospitalWuhan University of Science and TechnologyWuhan 430065China Department of CardiologyGuangdong Cardiovascular InstituteGuangdong Provincial Key Laboratory of Coronary Heart Disease PreventionGuangdong General HospitalGuangzhouChina College of PharmacyShanghai University of Medicine and Health SciencesShanghai 210000China
出 版 物：《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗（英文）)
年 卷 期：2023年第8卷第4期
页 面：1889-1900页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金：National Natural Science Foundation of China(#81770377,#82030007) Hubei Province Funds for Distinguished Young Scholars(#2020CFA076) High-level Hospital Construction Project(#DFJH201807) Scientific Research Plan Project of Hubei Provincial Department of Education(#D20211105) Health Commission of Hubei Province Scientific Research Project(#WJ2021M215)
主 题：diabetic endogenous cardiomyopathy
摘 要：In this study,we identified that a conserved circular RNA(circRNA)DICAR,which was downregulated in diabetic mouse *** had an inhibitory effect on diabetic cardiomyopathy(DCM),as the spontaneous cardiac dysfunction,cardiac cell hypertrophy,and cardiac fibrosis occurred in DICAR deficiency(DICAR+/−)mice,whereas the DCM was alleviated in DICARoverexpressed DICARTg *** the cellular level,we found that overexpression of DICAR inhibited,but knockdown of DICAR enhanced the diabetic cardiomyocyte *** the molecular level,we identified that DICAR-VCP-Med12 degradation could be the underlying molecular mechanism in DICAR-mediated *** synthesized DICAR junction part(DICAR-JP)exhibited a similar effect to the entire *** addition,the expression of DICAR in circulating blood cells and plasma from diabetic patients was lower than that from health controls,which was consistent with the decreased DICAR expression in diabetic *** and the synthesized DICAR-JP may be drug candidates for DCM.
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