Evidence Details for Vdac1
PMID Title Journal Year Abstract
25302705 Electro-acupuncture at Neiguan pretreatment alters genome-wide gene expressions and protects rat myocardium against ischemia-reperfusion. Molecules. 2014 Oct 9;19(10):16158-78. doi: 10.3390/molecules191016158. 2014 Oct 9 This study investigated genome-wide gene expressions and the cardioprotective effects of electro-acupuncture pretreatment at the PC6 Neiguan acupoint on myocardial ischemia reperfusion (I/R) injury. Male SD rats were randomly divided into four groups: sham operation (SO), I/R, electro-acupuncture at the PC6 Neiguan acupoint pretreatment (EA) and electro-acupuncture at non-acupoint pretreatment (NA). Compared with the I/R group, the survival rate of the EA group was significantly increased, the arrhythmia score, infarction area, serum concentrations of CK, LDH and CK-Mb and plasma level of cTnT were significantly decreased. RNA-seq results showed that 725 genes were up-regulated and 861 genes were down-regulated under I/R conditions compared to the SO group; both EA and NA reversed some of these gene expression levels (592 in EA and 238 in NA group). KEGG pathway analysis indicated that these genes were involved in multiple pathways, including ECM, MAPK signaling, apoptosis, cytokine and leukocyte pathways. In addition, some pathways were uniquely regulated by EA, but not NA pretreatment, such as oxidative stress, cardiac muscle contraction, gap junction, vascular smooth muscle contraction, hypertrophic, NOD-like receptor, and P53 and B-cell receptor pathways. This study was first to reveal the gene expression signatures of acute myocardial I/R injury and electro-acupuncture pretreatment in rats."

Evidence Sentence: The role of VDAC1 and of the other isoforms VDAC2 and VDAC3 in cell death is multi-faceted and complex.
Evidence Sentence: Binding of anti-apoptotic Bcl-2 and BclxL to VDAC1 (with resulting inhibition of porin) has an anti-apoptotic action.
Evidence Sentence: In contrast, Bax-induced cytochrome c release was observed in mitochondria isolated from all WT, VDAC1-, VDAC3-, and VDAC1/VDAC3-null cells, suggesting a controversial consequence for Vdac3s function on apoptosis.