Baicalin Attenuates Diabetic Cardiomyopathy <i>In Vivo</i> and <i>In Vitro</i> by Inhibiting Autophagy and Cell Death Through SENP1/SIRT3 Signaling Pathway Activation
Peipei Zhang, Haowei Wu, Haifei Lou, Jiedong Zhou, Jinjin Hao, Hui Lin, Songqing Hu, Zuoquan Zhong, Juntao Yang, Hangyuan Guo, Jufang Chi
Abstract
Aims: Diabetic heart damage can lead to cardiomyocyte death, which endangers human health. Baicalin (BAI) is a bioactive compound that plays an important role in cardiovascular diseases. Sentrin/SUMO-specific protease 1 (SENP1) regulates the de-small ubiquitin-like modifier (deSUMOylation) process of Sirtuin 3 (SIRT3) and plays a crucial role in regulating mitochondrial mass and preventing cell injury. Our hypothesis is that BAI regulates the deSUMOylation level of SIRT3 through SENP1 to enhance mitochondrial quality control and prevent cell death, ultimately improving diabetic cardiomyopathy (DCM).
Topics & Concepts
AutophagyIn vivoDiabetic cardiomyopathySIRT3In vitroBaicalinCell biologyCardiomyopathySignal transductionChemistryProgrammed cell deathCancer researchMedicinePharmacologyBiologyInternal medicineApoptosisBiochemistrySirtuinHeart failureChromatographyAcetylationHigh-performance liquid chromatographyGeneBiotechnologyParkinson's Disease Mechanisms and TreatmentsAutophagy in Disease and TherapySirtuins and Resveratrol in Medicine