Evidence map›Paper›PMID 39104320›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024

Enhanced glycolysis causes extracellular acidification and activates acid-sensing ion channel 1a in hypoxic pulmonary hypertension.

Megan N Tuineau, Lindsay M Herbert, Selina M Garcia, Thomas C Resta, Nikki L Jernigan

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 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.
Selina M GarciaDepartment of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.ORCID 0000-0002-7792-8371
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
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) 24PRE1196925HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01 HL-111084HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) T32 HL-007736NHLBI NIH HHS F31 HL170503NHLBI NIH HHS R01 HL111084NHLBI NIH HHS R01 HL169945NHLBI NIH HHS T32 HL007736NIGMS NIH HHS P20 GM121176
6 · The paper itself

Abstract

In pulmonary hypertension (PHTN), a metabolic shift to aerobic glycolysis promotes a hyperproliferative, apoptosis-resistant phenotype in pulmonary arterial smooth muscle cells (PASMCs). Enhanced glycolysis induces extracellular acidosis, which can activate proton-sensing membrane receptors and ion channels. We previously reported that activation of the proton-gated cation channel acid-sensing ion channel 1a (ASIC1a) contributes to the development of hypoxic PHTN. Therefore, we hypothesize that enhanced glycolysis and subsequent acidification of the PASMC extracellular microenvironment activate ASIC1a in hypoxic PHTN. We observed decreased oxygen consumption rate and increased extracellular acidification rate in PASMCs from chronic hypoxia (CH)-induced PHTN rats, indicating a shift to aerobic glycolysis. In addition, we found that intracellular alkalization and extracellular acidification occur in PASMCs following CH and in vitro hypoxia, which were prevented by the inhibition of glycolysis with 2-deoxy-d-glucose (2-DG). Inhibiting H

Indexed as

Acid Sensing Ion ChannelsGlycolysisHypertension, PulmonaryHypoxiaMyocytes, Smooth MusclePulmonary ArteryAcidosisAnimalsHydrogen-Ion ConcentrationMaleMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersRatsRats, Sprague-DawleySodium-Hydrogen Exchanger 1SymportersAcid Sensing Ion ChannelsAsic1 protein, ratMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersSlc9a1 protein, ratSodium-Hydrogen Exchanger 1Symportersmonocarboxylic acid transporterspH regulationvascular smooth muscleVB124Warburg effect

Identifiers

PMID39104320
PMCPMC11482464

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.