5/28/2023 0 Comments Where the heart leadsUnfortunately, it is estimated that close to half of asymptomatic/normotensive patients with well-controlled diabetes have cardiac dysfunction. Cardiac dysfunction is often silent in diabetic patients and not detected until later stages. This unique disease entity is presented as left ventricular dysfunction, independent of atherosclerosis, coronary heart disease, or hypertension. In conclusion, these studies show that cardiomyocyte MyD88 plays an apathogenetic role in DCM and Sch B specifically targets MyD88 to reduce inflammatory DCM.ĭiabetic cardiomyopathy (DCM) is a prevalent diabetes-induced secondary complication that leads to heart failure. Cardiomyocyte-specific MyD88 knockout also protects mice against cardiac inflammation and injury in type 1 diabetic mice. Treatment of type 1 and type 2 diabetic mice with Sch B protects heart function, reduces myocardial injuries, and decreases secretion of inflammatory cytokines. Inhibiting or silencing MyD88 is associated with reduced levels of HG-induced inflammatory cytokines and myocardial injuries in vitro. Further studies indicate that Sch B directly binds to and inhibits MyD88 activation, but does not alter MyD88-independent Toll-like receptor signaling in vivo and in vitro. RNA sequencing and inflammatory qPCR microarray show that Sch B mainly affects myeloid differentiation primary response 88 (MyD88)-dependent inflammatory gene expression in HG-challenged cardiomyocytes. It is shown that Sch B prevents high-level glucose (HG)-induced hypertrophic and fibrotic responses in cultured cardiomyocytes. In this study, the authors explore the pharmacological effects and mechanisms of Schisandrin B (Sch B), a natural compound with anti-inflammatory activity against DCM. Targeting key proteins in inflammatory signaling may provide new therapy for DCM. Diabetes manifests as chronic inflammation and leads to the development diabetic cardiomyopathy (DCM).
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