Review Article

Ion Channels and Oxidative Stress as a Potential Link for the Diagnosis or Treatment of Liver Diseases

Table 2

Ion channels involved in oxidative stress in the liver.

Ion channelPathologyModelOxidative stress effectReference

Kv2.1HepatomaHuh-7 cell line HCV inhibits Kv2.1, suppressing apoptosis in response to oxidative stress.[24]

Kir6.2Acute liver injuryLPS-induced mouse model of liver injuryKir6.2 knockout exacerbates LPS-induced endoplasmic reticulum stress in the liver.[207]

TRPM2Acetaminophen-induced liver damageTRPM2 KO miceH2 and acetaminophen-activated Ca2+ entry is attenuated in TRPM2 KO mouse hepatocytes.[208]

TRPM7Liver fibrosisRat hepatic stellate cellsBlockage of TRPM7 causes HSC death induced by ER stress-mediated apoptosis.[138]

TRPV4Liver fibrosisHuman liver fibrotic tissues
HSC-T6 cells
Rat liver fibrosis model, CCl4
TRPV4 expression correlates with HSC activation and in HSC-T6 induction of α-SMA and Col1α1. [144]

P2Y Liver fibrosisRat liver fibrosis model, CCl4Blockage of P2Y receptors inhibited CCl4-induced liver fibrosis in rats.[131]

P2X7Liver fibrosis
NASH
Mouse liver fibrosis model, CCL4
Mouse diet-induced obesity (DIO)
P2X7 blockage attenuates mouse liver fibrosis and P2X7 gene-deleted mice decreased α-SMA, Col1α1, and TGF-β1 in DIO treated mice.[117, 133]

CLIC1HepatocarcinomaMouse hepatocarcinoma ascites cell line (Hca-F)Overexpression of CLIC1 contributes to cell proliferation, apoptosis, migration, and invasion.[170]

ASIC1aLiver fibrosisRat liver fibrosis model, CCl4ASIC1a increases in HSC and inhibition of ASIC1a suppresses PDGF-induced profibrogenic effects of activated HSC.[160]

VSORHepatomaRat hepatoma (HTC) cellsActivated by H2O2 regulating cell volume and cell proliferation.[170]

VDACAcute ethanol intoxicationRat primary hepatocytesBax interacts with the PTP component protein VDAC and likely causes PTP opening, cytochrome c release, caspase activation, and apoptosis.[209]