Evidence map›Paper›PMID 38591063›Full record

ArticleJournal of translational internal medicine2024

WWP2 protects against sepsis-induced cardiac injury through inhibiting cardiomyocyte ferroptosis.

Zhi Li, Boquan Wu, Jie Chen, Ning Ye, Rui Ma, Chunyu Song, Yingxian Sun, Xingang Zhang, Guozhe Sun

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Journal of translational internal medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

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  18. Portrait of WWP1: the current state in human cancer.Frontiers in cell and developmental biology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Zhi LiDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Boquan WuDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Jie ChenDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Ning YeDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Rui MaDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Chunyu SongDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Yingxian SunDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Xingang ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.
Guozhe SunDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, 110001, Liaoning Province, China.ORCID https://orcid.org/0000-0002-8373-1049
First Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Objectives: Cardiac injury plays a critical role in contributing to the mortality associated with sepsis, a condition marked by various forms of programmed cell deaths. Previous studies hinted at the WW domain-containing E3 ubiquitin protein ligase 2 (WWP2) involving in heart failure and endothelial injury. However, the precise implications of WWP2 in sepsis-induced cardiac injury, along with the underlying mechanisms, remain enigmatic. Methods: Sepsis induced cardiac injury were constructed by intraperitoneal injection of lipopolysaccharide. To discover the function of WWP2 during this process, we designed and performed loss/gain-of-function studies with cardiac-specific vectors and WWP2 knockout mice. Combination experiments were performed to investigate the relationship between WWP2 and downstream signaling in septic myocardium injury. Results: The protein level of WWP2 was downregulated in cardiomyocytes during sepsis. Cardiac-specific overexpression of WWP2 protected heart from sepsis induced mitochondrial oxidative stress, programmed cell death and cardiac injury, while knockdown or knockout of WWP2 exacerbated this process. The protective potency of WWP2 was predominantly linked to its ability to suppress cardiomyocyte ferroptosis rather than apoptosis. Mechanistically, our study revealed a direct interaction between WWP2 and acyl-CoA synthetase long-chain family member 4 (FACL4), through which WWP2 facilitated the ubiquitin-dependent degradation of FACL4. Notably, we observed a notable reduction in ferroptosis and cardiac injury within WWP2 knockout mice after FACL4 knockdown during sepsis. Conclusions: WWP2 assumes a critical role in safeguarding the heart against injury induced by sepsis via regulating FACL4 to inhibit LPS-induced cardiomyocytes ferroptosis.

Indexed as

cardiac injuryferroptosisoxidative stresssepsisWW domain-containing E3 ubiquitin protein ligase 2

Identifiers

PMID38591063
PMCPMC11000860
OpenAlexW4393033669

What OpenQuestion holds

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LicenceCC BY
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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.