Evidence map›Paper›PMID 39937832›Full record

ArticlePloS one2025

Upregulated LIMD1 alleviates pressure overload-induced cardiac hypertrophy via inhibits YAP1/AKT/GSK3β signaling.

Fengwen Xie, Bin Yuan, Ye Zhang, Liru Chen, Yingmei Zhong, Quan Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 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. Article
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

6 authors.

Fengwen XieDepartment of Thoracic Surgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Bin YuanDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Ye ZhangDepartment of Thoracic Surgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Liru ChenDepartment of Thoracic Surgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Yingmei ZhongDepartment of Thoracic Surgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.
Quan XuDepartment of Thoracic Surgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, China.ORCID 0000-0001-9604-7601

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesPathological cardiac hypertrophy plays a significant role in the development and progression of heart failure (HF). LIM Domain Containing 1 (LIMD1) serves as a crucial regulatory factor in protein-protein interactions during cellular signal transduction. This study aims to investigate the specific roles and mechanisms of LIMD1 in pathological cardiac remodeling.

methodsWe employed an adeno-associated virus 9 (AAV9) system to overexpress LIMD1 in the hearts through tail vein injection. C57BL/6 mice underwent transverse aortic constriction (TAC) for four weeks. Cardiac function was assessed using echocardiography, while cardiac remodeling was evaluated through histopathology and molecular techniques.

resultsOur findings demonstrated elevated levels of LIMD1 in murine hearts subjected to TAC treatment and H9c2 cells challenged with angiotensin II (Ang II). Compared with wild-type (WT) mice, those injected with AAV-9-LIMD1 exhibited significantly reduced TAC-induced cardiac dysfunction, hypertrophy, and fibrosis. Mechanistically, both in vitro and in vivo experiments suggested that the beneficial effects of LIMD1 might be associated with the inhibition of the YAP1/AKT/GSK3β signaling pathway.

conclusionIn summary, this study is the first to demonstrate the protective effects of LIMD1 against TAC-induced pathological cardiac remodeling. These effects are attributed to the inhibition of the YAP1/AKT/GSK3β signaling pathway.

Indexed as

Adaptor Proteins, Signal TransducingCardiomegalyGlycogen Synthase Kinase 3 betaIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsProto-Oncogene Proteins c-aktSignal TransductionAngiotensin IIAnimalsCell Cycle ProteinsCell LineMaleMiceMice, Inbred C57BLRatsTranscription FactorsAdaptor Proteins, Signal TransducingAngiotensin IICell Cycle ProteinsGlycogen Synthase Kinase 3 betaGsk3b protein, mouseIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsProto-Oncogene Proteins c-aktTranscription FactorsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID39937832
PMCPMC11819601

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.