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Currently, there is no specific treatment for DCM. Studies have proved that mitochondrial dysfunction and endoplasmic reticulum (ER) stress are key factors for the development and progression of DCM. The mitochondria\u2010associated ER membranes (MAMs) are a unique domain formed by physical contacts between mitochondria and ER and mediate organelle communication. Under high glucose conditions, changes in the distance and composition of MAMs lead to abnormal intracellular signal transduction, which will affect the physiological function of MAMs, such as alter the Ca<jats:sup>2+<\/jats:sup> homeostasis in cardiomyocytes, and lead to mitochondrial dysfunction and abnormal apoptosis. Therefore, the dysfunction of MAMs is closely related to the pathogenesis of DCM. In this review, we summarized the evidence for the role of MAMs in DCM and described that MAMs participated directly or indirectly in the regulation of the pathophysiological process of DCM via the regulation of Ca<jats:sup>2+<\/jats:sup> signaling, mitochondrial dynamics, ER stress, autophagy, and inflammation. Finally, we discussed the clinical transformation prospects and technical limitations of MAMs\u2010associated proteins (such as MFN2, FUNDC1, and GSK3<jats:italic>\u03b2<\/jats:italic>) as potential therapeutic targets for DCM.<\/jats:p>","DOI":"10.1155\/2022\/2531458","type":"journal-article","created":{"date-parts":[[2022,4,12]],"date-time":"2022-04-12T00:05:34Z","timestamp":1649721934000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Mitochondria\u2010Endoplasmic Reticulum Contacts: The Promising Regulators in Diabetic 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