Evidence map›Paper›PMID 35682884›Full record

ReviewInternational journal of molecular sciences2022

AMPK and the Challenge of Treating Hypoxic Pulmonary Hypertension.

Karen Flores, Patricia Siques, Julio Brito, Silvia M Arribas

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.8field-weighted citation impact, top 5% of its field
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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Polygonum cuspidatum Exosome-Like Nanovesicles Alleviate Hypoxic Pulmonary Hypertension by Stabilizing PON1 to Inhibit MAPK-Mediated PASMC Phenotypic Switching.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  9. New Insights into Mitochondria in Health and Diseases.International journal of molecular sciences · 2024
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  14. Effects of the peripheral CBFrontiers in pharmacology · 2022
    Article
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  16. The role and mechanism of AMPK in pulmonary hypertension.Therapeutic advances in respiratory disease
    Review
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

4 authors at 2 institutions in 2 countries.

Karen FloresInstitute of Health Studies, University Arturo Prat, Av. Arturo Prat 2120, Iquique 1110939, Chile.
Patricia SiquesInstitute of Health Studies, University Arturo Prat, Av. Arturo Prat 2120, Iquique 1110939, Chile.ORCID 0000-0002-4963-195X
Julio BritoInstitute of Health Studies, University Arturo Prat, Av. Arturo Prat 2120, Iquique 1110939, Chile.ORCID 0000-0002-0050-8774
Silvia M ArribasDepartment of Physiology, University Autonoma of Madrid, 28049 Madrid, Spain.
Arturo Prat University · CLUniversidad Autónoma de Madrid · ES

Funding

GORE-FIC TARAPACA BIP30477541-0 / GORE-FIC TARAPACA BIP30487388-0 BIP30477541-0 / BIP30487388-0
6 · The paper itself

Abstract

Hypoxic pulmonary hypertension (HPH) is characterized by sustained elevation of pulmonary artery pressure produced by vasoconstriction and hyperproliferative remodeling of the pulmonary artery and subsequent right ventricular hypertrophy (RVH). The search for therapeutic targets for cardiovascular pathophysiology has extended in many directions. However, studies focused on mitigating high-altitude pulmonary hypertension (HAPH) have been rare. Because AMP-activated protein kinase (AMPK) is involved in cardiovascular and metabolic pathology, AMPK is often studied as a potential therapeutic target. AMPK is best characterized as a sensor of cellular energy that can also restore cellular metabolic homeostasis. However, AMPK has been implicated in other pathways with vasculoprotective effects. Notably, cellular metabolic stress increases the intracellular ADP/ATP or AMP/ATP ratio, and AMPK activation restores ATP levels by activating energy-producing catabolic pathways and inhibiting energy-consuming anabolic pathways, such as cell growth and proliferation pathways, promoting cardiovascular protection. Thus, AMPK activation plays an important role in antiproliferative, antihypertrophic and antioxidant pathways in the pulmonary artery in HPH. However, AMPK plays contradictory roles in promoting HPH development. This review describes the main findings related to AMPK participation in HPH and its potential as a therapeutic target. It also extrapolates known AMPK functions to discuss the less-studied HAPH context.

Indexed as

AMP-Activated Protein KinasesHypertension, PulmonaryAdenosine TriphosphateAltitude SicknessHumansHypoxiaPulmonary ArteryAdenosine TriphosphateAMP-Activated Protein KinasesAMPKcardioprotectionhigh altitudehypoxic pulmonary hypertension

Identifiers

PMID35682884
PMCPMC9181235
OpenAlexW4281850484

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.