Evidence map›Paper›PMID 41740252›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2026

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

Megan N Tuineau, Lindsay M Herbert, Heaven E Medina, Jay S Naik, Thomas C Resta, Nikki L Jernigan

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Megan N TuineauDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.ORCID 0000-0002-1921-7539
Lindsay M HerbertDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.
Heaven E MedinaDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.
Jay S NaikDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.ORCID 0000-0002-5725-4664
Thomas C RestaDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.ORCID 0000-0002-7219-6159
Nikki L JerniganDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.ORCID 0000-0001-6269-2274

Funding

Unfolded Protein Response and Autophagy in T Helper Cell Effector FunctionP20GM121176 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI VOJO P DERETIC · 2017 to 2026
$24.9M
MINORITY INSTITUTIONAL RESEARCH TRAINING PROGRAM (T32)T32HL007736 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI RESTA, THOMAS C · 1993 to 2025
$6.5M
Vascular Smooth Muscle Function in Pulmonary HypertensionR01HL111084 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI JERNIGAN, NIKKI L · 2013 to 2022
$3.4M
Oxidant Signaling in Pulmonary HypertensionR01HL169945 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI THOMAS C RESTA · 2023 to 2026
$2.3M
Regulation of H2S signaling in vascular functionR01HL160606 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI NAIK, JAY S · 2022 to 2025
$2.1M
The Role of Mitochondrial Acid-Sensing Ion Channel 1 in Pulmonary HypertensionF31HL170503 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI TUINEAU, MEGAN · 2024 to 2025
$62k
American Heart Association (AHA) 18TPA34110281American Heart Association (AHA) 24PRE1196925American Heart Association (AHA) 24SURE1331678HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) F31 HL-170503HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 HL-111084HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 HL-160606HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 HL-169945HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) T32 HL-007736NHLBI NIH HHS F31 HL170503NHLBI NIH HHS R01 HL111084NHLBI NIH HHS R01 HL160606NHLBI NIH HHS R01 HL169945NHLBI NIH HHS T32 HL007736NIGMS NIH HHS P20 GM121176
6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a progressive vascular disease driven by pulmonary arterial remodeling, characterized by cellular hyperproliferation, resistance to apoptosis, and phenotypic plasticity. Our laboratory has shown that the proton-gated cation channel, acid-sensing ion channel 1a (ASIC1a), is essential for the development of chronic hypoxia (CH)-induced PH in rodents. Importantly, ASIC1a activation occurs without changes in total ASIC1a levels but reflects a hypoxia-dependent redistribution to the plasma membrane in pulmonary arterial smooth muscle cells (PASMCs). In neurons, mitochondrial-localized ASIC1a (mtASIC1a) contributes to oxidative stress-induced mitochondrial membrane potential (ΔΨm) depolarization and apoptosis. Although mtASIC1a has not been described in vascular cells, its role in PASMCs may be relevant to mitochondrial dysfunction and apoptosis resistance in PH. We hypothesize that mtASIC1a is a crucial regulator of PASMC mitochondrial homeostasis, and its loss following CH promotes mitochondrial dysfunction and apoptosis resistance. Consistent with this, mtASIC1a localization was decreased in PASMCs and intrapulmonary arteries from CH rats compared with controls. Functionally, PASMCs from CH rats or

Indexed as

Acid Sensing Ion ChannelsMitochondriaMuscle, Smooth, VascularMyocytes, Smooth MusclePulmonary ArteryAnimalsApoptosisHypertension, PulmonaryHypoxiaMaleMembrane Potential, MitochondrialMiceRatsRats, Sprague-DawleyAcid Sensing Ion ChannelsAsic1 protein, ratapoptosismitochondriamitochondrial membrane potentialmitophagypulmonary hypertension

Identifiers

PMID41740252
PMCPMC13074392

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.