Evidence map›Paper›PMID 40723901›Full record

ArticleBiomolecules2025

Targeted Overexpression of Mitochondrial ALDH2 in Coronary Endothelial Cells Mitigates HFpEF in a Diabetic Mouse Model.

Guodong Pan, Bipradas Roy, Emmanuel Oppong Yeboah, Thomas Lanigan, Roland Hilgarth, Rajarajan A Thandavarayan, Michael C Petriello, Shailendra Giri, Suresh Selvaraj Palaniyandi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Guodong PanDivision of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202, USA.ORCID 0000-0003-0594-4492
Bipradas RoyDivision of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202, USA.ORCID 0000-0001-6472-951X
Emmanuel Oppong YeboahDivision of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202, USA.ORCID 0009-0007-6453-3112
Thomas LaniganVector Core, Biomedical Research Core Facilities, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Roland HilgarthVector Core, Biomedical Research Core Facilities, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Rajarajan A ThandavarayanDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX 77030, USA.ORCID 0000-0001-8452-2903
Michael C PetrielloInstitute of Environmental Health Sciences, Wayne State University, Detroit, MI 48202, USA.ORCID 0000-0002-5583-8092
Shailendra GiriDepartment of Neurology, Henry Ford Health, Detroit, MI 48202, USA.ORCID 0000-0002-7123-829X
Suresh Selvaraj PalaniyandiDivision of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202, USA.

Funding

Pilot and Feasibility ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2022 to 2025
$4.9M
American Heart Association 835262Henry Ford Health System A10249MDRC-National Institute of Diabetes and Digestive and Kidney Diseases P30DK020572NHLBI NIH HHS 1R01HL139877-01A1NIDDK NIH HHS P30 DK020572NIEHS NIH HHS R21 ES033813NIEHS NIH HHS R21 ES033813-01A1
6 · The paper itself

Abstract

Heart failure (HF) has become an epidemic, with a prevalence of ~7 million cases in the USA. Despite accounting for nearly 50% of all HF cases, heart failure with a preserved ejection fraction (HFpEF) remains challenging to treat. Common pathophysiological mechanisms in HFpEF include oxidative stress, microvascular dysfunction, and chronic unresolved inflammation. Our lab focuses on oxidative stress-mediated cellular dysfunction, particularly the toxic effects of lipid peroxidation products like 4-hydroxy-2-nonenal (4HNE). Aldehyde dehydrogenase 2 (ALDH2), a mitochondrial enzyme, plays a vital role in detoxifying 4HNE and thereby protecting the heart against pathological stress. ALDH2 activity is reduced in various metabolic stress-mediated cardiac pathologies. The dysfunction of coronary vascular endothelial cells (CVECs) is critical in initiating HFpEF development. Thus, we hypothesized that ectopic overexpression of ALDH2 in CVECs could mitigate metabolic stress-induced HFpEF pathogenesis. In this study, we tested the efficacy of intracardiac injections of the

Indexed as

Aldehyde Dehydrogenase, MitochondrialDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Endothelial CellsHeart FailureMitochondriaAnimalsCoronary VesselsDisease Models, AnimalMaleMiceMice, Inbred C57BLOxidative StressStroke VolumeAldehyde Dehydrogenase, MitochondrialALDH2 protein, mouse4-hydroxy-2-nonenal (4HNE)adeno-associated virus serotype 9 expressing vascular endothelial (VE)-cadherinaldehyde dehydrogenase 2 (ALDH2)coronary vascular endothelial cells (CVECs)gene transferheart failure with preserved ejection fraction (HFpEF)type 2 diabetes mellitus (T2DM)

Identifiers

PMID40723901
PMCPMC12293769

What Socratic 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 Socratic graph.