Mitochondrial acid-sensing ion channel 1a deficiency induces mitochondrial dysfunction in pulmonary arterial smooth muscle cells

American Journal of Physiology-Lung Cellular and Molecular Physiology 2026

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Authors: Megan N. Tuineau, Lindsay M. Herbert, Heaven E. Medina, Jay Naik, Thomas C. Resta, Nikki L. Jernigan
DOI: 10.1152/ajplung.00324.2025
Cited by: 2
References: 69

Abstract

This study identifies mitochondrial acid-sensing ion channel 1a (mtASIC1a) as a novel regulator of mitochondrial homeostasis in pulmonary arterial smooth muscle cells (PASMCs). Critically, mtASIC1a deficiency in PASMCs following in vivo chronic hypoxia or genetic deletion promotes mitochondrial membrane potential (ΔΨm) hyperpolarization, Ca 2+ and superoxide (O 2 − ) accumulation, impaired mitophagy, and caspase inhibition. Restoring mtASIC1a by lentiviral transduction prevents ΔΨm hyperpolarization and restores caspase cleavage, highlighting its importance in mitochondrial signaling and hypoxic pulmonary hypertension pathophysiology.

Fields of Study & Subjects

Ion Transport and Channel Regulation Mitochondrial Function and Pathology Pulmonary Hypertension Research and Treatments

Publication details

Journal / source
American Journal of Physiology-Lung Cellular and Molecular Physiology
Publisher
American Physiological Society
Volume
330
Issue
4
Pages
L390–L403
Publication date
25 February 2026
Language
EN