Acid-sensing ion channel 1a promotes alcohol-associated liver disease in mice via regulating endoplasmic reticulum autophagy.

Alcohol-associated liver disease (ALD) is a hepatocyte dysfunction disease caused by chronic or excessive alcohol consumption, which can lead to extensive hepatocyte necrosis and even liver failure. Currently, the pathogenesis of ALD and the anti-ALD mechanisms have not been fully elucidated yet. In this study, we investigated the effects of endoplasmic reticulum autophagy (ER-phagy) in ALD and the role of acid-sensing ion channel 1a (ASIC1a) in ER stress-mediated ER-phagy.

Kupffer cell pyroptosis mediated by METTL3 contributes to the progression of alcoholic steatohepatitis.

Chronic alcohol consumption is a major risk factor for alcoholic steatohepatitis (ASH). Previous studies have shown that direct injury of hepatocytes is the key factor in its occurrence and development. However, our study shows that the role of Kupffer cells in ASH cannot be ignored.

Acid-sensitive ion channel 1a regulates TNF-α expression in LPS-induced acute lung injury via ERS-CHOP-C/EBPα signaling pathway.

Background: Acute lung injury (ALI) is the local inflammatory response of the lungs involved in a variety of inflammatory cells. Macrophages are immune cells and inflammatory cells widely distributed in the body. Acid-sensitive ion channel 1a (ASIC1a) is involved in the occurrence of ALI, but the mechanism is still unclear.

N-phenethyl-5-phenylpicolinamide alleviates inflammation in acute lung injury by inhibiting HIF-1α/glycolysis/ASIC1a pathway.

Aims: Acute lung injury (ALI) is triggered by an acute inflammatory response. Lipopolysaccharide (LPS) is recognized as an important participant in the pathogenesis of sepsis, which may induce ALI. N-phenethyl-5-phenylpicolinamide (N5P) is a newly synthesized HIF-1α inhibitor.

Recent Advances in Acid-sensitive Ion Channels in Central Nervous System Diseases.

Acid-sensitive ion channels (ASICs) are cationic channels activated by extracellular protons and widely distributed in the nervous system of mammals. It belongs to the ENaC/DEG family and has four coding genes: ASIC1, ASIC2, ASIC3, and ASIC4, which encode eight subunit proteins: ASIC1a, ASIC1b, ASIC1b2, ASIC2a, ASIC2b, ASIC3, ASIC4, and ASIC5. Different subtypes of ASICs have different distributions in the central nervous system, and they play an important role in various physiological and pathological processes of the central nervous system, including synaptic plasticity, anxiety disorders, fear conditioning, depressionrelated behavior, epilepsy, Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, malignant Glioma, pain, and others.

Inonotsuoxide B regulates M1 to M2 macrophage polarization through sirtuin-1/endoplasmic reticulum stress axis.

We explored the effect of tetracyclic triterpenoid inonotsuoxide B (IB) extracts of Inonotus obliquus on M1 to M2 macrophage polarization and its possible underlying mechanism. Lipopolysaccharide (LPS)-activated M1 macrophages exert pro-inflammatory effects and release inflammatory cytokines including interleukin (IL)-1β and tumor necrosis factor (TNF)-α. The model and various groups were treated with different IB concentrations (2.

The interaction of ASIC1a and ERS mediates nerve cell apoptosis induced by insulin deficiency.

Diabetes-related brain complications are the most serious complications of terminal diabetes. The increasing evidence have showed that the predisposing factor is not only hyperglycemia, but also insulin deficiency. In this study, we demonstrated that insulin deficiency was involved in the apoptosis of nerve cells, and it was related to the interaction between acid-sensitive ion channel 1a (ASIC1a) and endoplasmic reticulum stress (ERS).

ASIC1a regulates miR-350/SPRY2 by N -methyladenosine to promote liver fibrosis.

As a reversible scar repair reaction, liver fibrosis can be blocked or even reversed by proper intervention during its formation. Our work suggests that acid-sensitive ion channel 1a (ASIC1a) participates in liver fibrosis and presents a novel mechanism involving m A modification and miR-350/SPRY2. We demonstrated that the expression of ASIC1a was significantly increased in liver tissue of patients with liver fibrosis and animal models of liver fibrosis, as well as PDGF-BB-induced activated HSC-T6.

PI3-kinase/Akt pathway-regulated membrane transportation of acid-sensing ion channel 1a/Calcium ion influx/endoplasmic reticulum stress activation on PDGF-induced HSC Activation.

Acid-sensing ion channel 1a (ASIC1a) allows Na and Ca flow into cells. It is expressed during inflammation, in tumour and ischaemic tissue, in the central nervous system and non-neuronal injury environments. Endoplasmic reticulum stress (ERS) is caused by the accumulation of misfolded proteins that interferes with intracellular calcium homoeostasis.