Key result
Targeting mitochondria-associated membranes restores calcium handling in diabetic cardiomyopathy.
Why the study?
Mitochondria-associated membranes have attracted attention for maintaining myocardial calcium homeostasis in diabetic cardiomyopathy, prompting a review of the underlying signaling pathways and targeted pharmacological interventions to inform mechanistic research and drug development.
Does targeting the MAM–calcium homeostasis axis with agents such as dapagliflozin, ferulic acid, quercetin, and ginsenoside Rb1 improve diabetic cardiomyopathy?
Does targeting the MAM–calcium homeostasis axis with agents such as dapagliflozin, ferulic acid, quercetin, and ginsenoside Rb1 improve diabetic cardiomyopathy?
Answers are grounded in this paper and cite their sources.
This review summarizes the molecular mechanisms by which mitochondria-associated membranes regulate calcium homeostasis in diabetic cardiomyopathy and highlights potential therapeutic agents such as dapagliflozin that target this pathway.
Diabetic cardiomyopathy (DCM) is a highly specific cardiovascular complication of diabetes that occurs independently of hypertension and coronary atherosclerotic heart disease, and is primarily characterized by diffuse myocardial fibrosis and impaired diastolic and systolic function. In recent years, mitochondria-associated membranes (MAMs), as dynamic membrane contact points connecting the endoplasmic reticulum and mitochondria, have attracted much attention in maintaining calcium homeostasis in myocardial cells, regulating energy metabolism and cell survival fate. This article systematically reviews the structural composition of MAMs and their core roles in apoptosis, mitophagy, inflammatory response and calcium homeostasis regulation. It focuses on the molecular mechanisms by which FUNDC1/IP3R2, Bmal1/Bcl-2/IP3R and PPARα/Mfn2 MAM-related signaling pathways mediate calcium overload in DCM, and reviews the research progress of drugs such as dapagliflozin, ferulic acid, quercetin, and ginsenoside Rb1 in improving DCM by targeting the MAM–calcium homeostasis axis. Finally, this review discusses the key scientific issues and future translational research directions in this field, aiming to provide references for mechanism research and new drug development in DCM.
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孙静 et al. (2026) conducted a review in Diabetic cardiomyopathy (DCM). MAM-targeted therapies (dapagliflozin, ferulic acid, quercetin, ginsenoside Rb1) was evaluated. Mitochondria-associated membranes regulate myocardial calcium homeostasis via FUNDC1/IP3R2, Bmal1/Bcl-2/IP3R, and PPARα/Mfn2 pathways, serving as therapeutic targets in diabetic cardiomyopathy.
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