Abstract
Diabetic cardiomyopathy (DbCM) is a prevalent disease, characterized by contractile dysfunction and left ventricular hypertrophy. Patients with DbCM have high morbidity and mortality worldwide. Recent studies have identified that pyroptosis, a kind of cell death, could be induced by hyperglycemia involved in the formation of DbCM. This review summarizes the regulatory mechanisms of pyroptosis in DbCM, including NOD-like receptor3, AIM2 inflammasome, long non-coding RNAs, microRNAs, circular RNA, autophagy, and some drugs.
Highlights
Diabetes mellitus (DM) potentially causes increased risks of heart failure in the absence of the traditional impetus to heart failure such as hypertension and coronary heart disease, including, diabetic cardiomyopathy (DbCM) (Murtaza et al, 2019)
Previous and emerging studies indicated that the regulations of pyroptosis in DbCM are complicated with the involvement of NLRP3 and absent in melanoma 2 (AIM2) inflammasome, long non-coding RNAs, micro RNA, circular RNA, autophagy, and some drugs (Table 1)
Pyroptosis features the formation of membrane pore and leakage of proinflammatory intracellular contents such as IL-1β and IL18, which is mainly activated by caspase-1 signaling pathways
Summary
Diabetic cardiomyopathy (DbCM) is a prevalent disease, characterized by contractile dysfunction and left ventricular hypertrophy. Patients with DbCM have high morbidity and mortality worldwide. Recent studies have identified that pyroptosis, a kind of cell death, could be induced by hyperglycemia involved in the formation of DbCM. This review summarizes the regulatory mechanisms of pyroptosis in DbCM, including NODlike receptor, AIM2 inflammasome, long non-coding RNAs, microRNAs, circular RNA, autophagy, and some drugs. Reviewed by: Zhengyuan Xia, The University of Hong Kong, Hong Kong SAR, China John Reyes Ussher, University of Alberta, Canada
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