Exacerbated post‐infarct pathological myocardial remodelling in diabetes is associated with impaired autophagy and aggravated NLRP3 inflammasome activation

Background Diabetes mellitus (DM) patients surviving myocardial infarction (MI) have substantially higher mortality due to the more frequent development of subsequent pathological myocardial remodelling and concomitant functional deterioration. This study investigates the molecular pathways underlyi...

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Published in:ESC Heart Failure 2022-02, Vol.9 (1), p.303-317
Main Authors: Mao, Shuai, Chen, Peipei, Pan, Wenjun, Gao, Lei, Zhang, Minzhou
Format: Article
Language:English
Subjects:
Animals
Autophagy
Cardiac function
Cardiomyocytes
Coronary vessels
Cytokines
Diabetes
Diabetes Mellitus
Drug dosages
Heart failure
Humans
Inflammasomes - metabolism
Laboratory animals
Medical prognosis
Mice
Microscopy
Myocardial Infarction - metabolism
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
NLRP3 inflammasome
Original
Pathological myocardial remodelling
Surgery
Tumor necrosis factor-TNF
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Summary:Background Diabetes mellitus (DM) patients surviving myocardial infarction (MI) have substantially higher mortality due to the more frequent development of subsequent pathological myocardial remodelling and concomitant functional deterioration. This study investigates the molecular pathways underlying accelerated cardiac remodelling in a well‐established mouse model of diabetes exposed to MI. Methods and results Myocardial infarction in DM mice was established by ligating the left anterior descending coronary artery. Cardiac function was assessed by echocardiography. Myocardial hypertrophy and cardiac fibrosis were determined histologically 6 weeks post‐MI or sham operation. Autophagy, the NLRP3 inflammasome, and caspase‐1 were evaluated by western blotting or immunofluorescence. Echocardiographic imaging revealed significantly increased left ventricular dilation in parallel with increased mortality after MI in DM mice (53.33%) compared with control mice (26.67%, P 
ISSN:2055-5822
2055-5822
DOI:10.1002/ehf2.13754