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. 2020 Oct 9;21(20):7432. doi: 10.3390/ijms21207432

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Effect of hyperglycaemia on cardiomyocyte. (A) Under physiologic glucose levels, VDAC1 promotes mitochondrial calcium intake and buffering. (B) High glucose levels directly induce an increase of cytosolic calcium. Moreover, chronic hyperglycaemia causes mitochondrial NADPH overexpression and superoxide anion overproduction, thus promoting TSPO and VDAC1 overexpression. This, in turn, results in their probable interaction aimed to prevent mitochondrial calcium accumulation. On the other hand, enhanced cytosolic calcium promotes endoplasmic reticulum (ER) impairment, translocation of NT-MMP-2 from mitochondria-associated membrane (MAM) into mitochondrial matrix, and mitochondrial dysfunction.