Endoplasmic reticulum-mitochondria coupling attenuates vanadium-induced apoptosis via IP3R in duck renal tubular epithelial cells

Mulberry Leaf Polysaccharides Attenuate Oxidative Stress Injury in Peripheral Blood Leukocytes by Regulating Endoplasmic Reticulum Stress

“…The ER is a major organelle for Ca 2+ storage, while mitochondria are the main players in intracellular Ca 2+ uptake and apoptosis regulation, with Ca 2+ flow regulated between these two organelles by mitochondria-associated membranes (MAMs) [57]. Consequently, when Ca 2+ levels in the ER are disturbed, Ca 2+ may be released directly from the ER into the cytoplasm and possibly into the mitochondria through MAMs [58]. MAMs represent a 'bridge' between mitochondria and ER, while mfn2 and grp75 are crucial genes regulating this physical linkage, playing a major role in Ca 2+ transport [59].…”

“…MAMs represent a 'bridge' between mitochondria and ER, while mfn2 and grp75 are crucial genes regulating this physical linkage, playing a major role in Ca 2+ transport [59]. Over-expressions of mfn2 and grp75 in duck renal tubular epithelial cells led to excessive entry of Ca 2+ into mitochondria, thereby stimulating the release of pro-apoptotic factors and inducing apoptosis [58]. Consistent with the HP group, mfn2, grp75, vdac-1, mcu, and bax expressions were significantly increased compared with the NC group.…”

Inhibition of calcium imbalance protects hepatocytes from vanadium exposure-induced inflammation by mediating mitochondrial-associated endoplasmic reticulum membranes in ducks

“…Transmission electron microscopy ( TEM ) was applied for hepatocyte ultrastructural analysis after V and 2-APB exposure for 24 h, and the observation method was performed according to previous publications ( Peng et al, 2022 ).…”

“…The high expression of IP 3 R is accompanied by the enhancement of interactions between the IP 3 R-Grp75-VDAC1 complex and mitochondrial Ca 2+ overload ( Xu et al, 2018 ). A previous study showed that heavy metals could lead to mitochondrial impairment by inhibiting the regulation for the Ca 2+ conduction pathway in the ER, and eventually lead to MAMs dysfunction ( Peng et al, 2022 ). Studies have shown that Ca 2+ is actively released and exerts an integral role in the management of the inflammatory reaction by stimulating mitochondria and ER during inflammation.…”

Broadening horizons: the contribution of mitochondria-associated endoplasmic reticulum membrane (MAM) dysfunction in diabetic kidney disease

“…The flexibility of MAM protein assemblies allows for the recruitment of different signaling molecules based on specific cell states 31 , 32 . Resident proteins on the MAM are classified according to their different functions, for example, Ca 2+ transport-related protein: inositol 1,4,5-trisphosphate receptor (IP3R) 33 ; lipid synthesis and transfer-associated protein: phosphatidylserine synthase 1 and 2 (PSS1/2) 34 ; mitochondrial dynamic regulatory proteins: mitofusin 2 (MFN2), dynamin-related protein 1 (DRP1) 35 ; insulin signaling-related protein: protein kinase B (PKB), mammalian target of rapamycin complex (mTORC) 36 ; and so on. The presence of multifunctional proteomes in MAM indicates that they exert crucial roles in regulating cellular homeostasis and biological processes ( Table 1 ).…”