Abstract
Streptozotocin (STZ) at 35 mg/Kg was used to induce diabetes in rats. H9C2 cardiomyocytes and primary cardiomyocytes (PCM) were cultured at 5.5 and 50 mmol/L glucose, respectively. The expression levels of MALAT 1 and scorch death-related genes were detected by RT-PCR using plasmids to suppress or overexpress the related genes, respectively. Immunofluorescence, RT-PCR and Western blot were used to detect the extent of cell scorch death. MALAT 1 expression was elevated in diabetic and high glucose-induced cardiomyocytes and myocardial tissue from diabetic mice (p<0.001). Silencing of MALAT 1 alleviated cardiomyocyte scorch death by targeting NLRP3. Furthermore, silencing MALAT 1 reduced cell death and improved cardiac function and morphology. MALAT 1 is overexpressed in DCM and silencing MALAT 1 inhibits cell scorch death by affecting NLRP3 expression. We clarify for the first time that MALAT 1 may be a new therapeutic target for DCM.
Highlights
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus, often leading to heart failure, arrhythmias and sudden death
We demonstrate that Lncinflammation, and that the development of RNA MALAT 1 is overexpressed in a DCM model inflammation plays a crucial role in the development and that silencing MALAT 1 attenuates scorch death and progression of diabetic cardiomyopathy [4-6]
We found that the expression of Long-stranded non-coding RNA (LncRNA)-MALAT 1 in the serum of diabetic patients was significantly higher than that of healthy controls (Figure 1A, p
Summary
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus, often leading to heart failure, arrhythmias and sudden death. Silencing of MALAT 1 alleviated cardiomyocyte scorch death by targeting NLRP3. CONCLUSIONS: MALAT 1 is overexpressed in DCM and silencing MALAT 1 inhibits cell scorch death by affecting NLRP3 expression. We demonstrate that Lncinflammation, and that the development of RNA MALAT 1 is overexpressed in a DCM model inflammation plays a crucial role in the development and that silencing MALAT 1 attenuates scorch death and progression of diabetic cardiomyopathy [4-6]. Pyroptosis is the pro-inflammatory programmed induced cardiomyocytes and in STZ-induced death of cells [7]. It has the biochemical and diabetic mice. Our study suggests that MALAT 1 morphological characteristics of necrosis and may be a new therapeutic target for DCM. NLRP3 is activated during cellular focal death via the supramolecular complex focal death vesicle 14, which subsequently
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