Acid-sensing ion channel 1a modulation of apoptosis in acidosis-related diseases: implications for therapeutic intervention

Abstract

Acid-sensing ion channel 1a (ASIC1a), a prominent member of the acid-sensing ion channel (ASIC) superfamily activated by extracellular protons, is ubiquitously expressed throughout the human body, including the nervous system and peripheral tissues. Excessive accumulation of Ca2+ ions via ASIC1a activation may occur in the acidified microenvironment of blood or local tissues. ASIC1a-mediated Ca2+‑induced apoptosis has been implicated in numerous pathologies, including neurological disorders, cancer, and rheumatoid arthritis. This review summarizes the role of ASIC1a in the modulation of apoptosis via various signaling pathways across different disease states to provide insights for future studies on the underlying mechanisms and development of therapeutic strategies.

Membrane Dynamics and Cation Handling in Ferroptosis

“…A variety of channels participate in the process of Ca 2+ overload. These include Ca 2+ release channels such as IP 3 and ryanodine receptors, located in the endoplasmic reticulum, as well as storage-type Ca 2+ influx channels Orai1/Stim, acid-sensing ion channels (ASICs), and TRP channels, which are found in the plasma membrane ( 62 , 86 ). Mitochondrial Ca 2+ channels voltage-dependent anion channels (VDACs) and mitochondrial calcium uniporter (MCU) play major roles in transporting Ca 2 + across the outer and inner mitochondrial membranes, respectively ( 87 ).…”