Evidence map›Paper›PMID 40606520›Full record

ArticleJournal of molecular and cellular cardiology plus2025

Genetic deletion or pharmacological inhibition of acetyl-CoA carboxylase 2 enhances fatty acid oxidation and improves cardiac function and survival in the murine ATGL knockout model of severe heart failure.

Mai Usui, Yu Tsurekawa, Tatsuya Ikehara, Atsuyuki Shimazaki, Archana Vijayakumar, Robert P Myers, G Mani Subramanian, Eisuke Murakami

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular and cellular cardiology plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Mai UsuiDrug Discovery and Disease Research Laboratory, Shionogi & Co., Ltd., Osaka 561-0825, Japan.
Yu TsurekawaDrug Discovery and Disease Research Laboratory, Shionogi & Co., Ltd., Osaka 561-0825, Japan.
Tatsuya IkeharaDrug Discovery and Disease Research Laboratory, Shionogi & Co., Ltd., Osaka 561-0825, Japan.
Atsuyuki ShimazakiDrug Discovery and Disease Research Laboratory, Shionogi & Co., Ltd., Osaka 561-0825, Japan.
Archana VijayakumarOrsoBio, Inc., Menlo Park, CA 94025, USA.
Robert P MyersOrsoBio, Inc., Menlo Park, CA 94025, USA.
G Mani SubramanianOrsoBio, Inc., Menlo Park, CA 94025, USA.
Eisuke MurakamiOrsoBio, Inc., Menlo Park, CA 94025, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired myocardial energetics, including fatty acid oxidation (FAO), is a hallmark feature in the pathophysiology of various disorders. Deficiency of adipose triglyceride lipase (ATGL) results in impaired FAO which leads to severe heart failure due to massive triglyceride accumulation in cardiac muscle and coronary vasculature. Acetyl-CoA carboxylase 2 (ACC2) is a mitochondrial enzyme that regulates FAO; ACC2 inhibition increases transport of fatty acids into mitochondria for oxidation. In this study, the murine ATGL knockout (KO) model of severe heart failure was used to evaluate the effects ACC2 inhibition induced by whole body genetic KO (

Indexed as

ACC2Cardiac metabolismCardiovascular therapeuticsFatty acid oxidationTriglycerides

Identifiers

PMID40606520
PMCPMC12213096

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.