Altered VDAC-HK association and apoptosis in mouse peripheral blood lymphocytes exposed to diabetic condition: anin vitroandin vivostudy

Apoptosis regulation at the mitochondria membrane level

“…When bound to VDACs, HKs enable an effective coupling between oxidative phosphorylation (OXPHOS) and glycolysis by capturing ATP released from mitochondria for production of glucose-6-phosphate, the rate limiting step in the glycolytic cascade. Consequently, VDAC-HK interactions have drawn considerable interest as a potential pharmaceutical target for the development of novel anti-cancer agents [100]. A recent study has shown that high glucose may induce apoptosis via downregulation of HK2, leading to decreased interactions of HK2 with VDACs and increased VDACs-Bax association, with the subsequent increased release of cytochrome c [101].…”

Ca2+ Transportome and the Interorganelle Communication in Hepatocellular Carcinoma

“…Among its three isoforms (VDAC1, 2, 3), high expression of VDAC1 is associated with a negative outcome in terms of HCC [ 128 ]. VDAC1 directly interacts with the antiapoptotic Bcl2, hexokinase I (HK-I), and HK-II to protect cells against programmed cell death [ 129 ].…”

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“…[22] Hyperglycemia and insulin defi ciency are considered the two major etiopathogenic pillars of diabetes-associated immunodefi ciency (Figure 4) and susceptibility to infections. [153][154][155] Hyperglycemia as a primary trigger of pro-infl ammatory cytokine spillover [145] results in local and systemic infl ammation, and peripheral insulin resistance. [156,157] Increased levels of various infl ammatory markers and mediators-including white blood cell count, C-reactive protein, pro-infl ammatory cytokines and plasminogen activator inhibitor-1-are elevated in insulin resistant subjects and DMT2-aff ected patients.…”