Evidence map›Paper›PMID 40195212›Full record

ArticleJournal of cardiovascular translational research2025

IL-22 Attenuates Pressure Overload-Induced Heart Failure and Inflammation.

Lanqing Xiang, Guoqing Yin, Zifan Gong, Xian Lv, Cailin Feng, Lu Liu, Fuad A Abdu, Tingting Shi, Wen Zhang, Jiasuer Alifu and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 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

14 authors.

Lanqing Xiang *Department of Cardiology, Clinical Medical College of Shanghai Tenth People'S Hospital, Nanjing Medical University, Shanghai, China.
Guoqing Yin *Department of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Zifan GongThe Second Clinical Medical School of Nanjing Medical University, Nanjing, China.
Xian LvDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Cailin FengDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Lu LiuDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Fuad A AbduDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Tingting ShiDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Wen ZhangDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Jiasuer AlifuDepartment of Cardiology, Shanghai Tenth People'S Hospital, Tongji University School of Medicine, Shanghai, China.
Xiaojiang XuDepartment of Pathology & Laboratory Medicine, School of Medicine, Tulane University, New Orleans, LA, 70112, USA.
Yuxiang DaiDepartment of Cardiology, State Key Laboratory of Cardiovascular Diseases, Shanghai Institute of Cardiovascular Diseases, NHC Key Laboratory of Ischemic Heart Diseases China, Zhongshan Hospital, Fudan University, Shanghai, China. dai.yuxiang@hotmail.com.
Wenliang CheDepartment of Cardiology, Clinical Medical College of Shanghai Tenth People'S Hospital, Nanjing Medical University, Shanghai, China. chewenliang@tongji.edu.cn.
Xinyu WengDepartment of Cardiology, State Key Laboratory of Cardiovascular Diseases, Shanghai Institute of Cardiovascular Diseases, NHC Key Laboratory of Ischemic Heart Diseases China, Zhongshan Hospital, Fudan University, Shanghai, China. xyweng@fudan.edu.cn.ORCID 0000-0002-7620-0813

Funding

National Key Research and Development Project of China 2021YFC250050National Key Research and Development Project of China 2023YFC2506500National Natural Science Foundation of China 82100395National Natural Science Foundation of China 82370357Program of Shanghai Academic Research Leader 22XD1423300
6 · The paper itself

Abstract

Heart failure (HF) due to left ventricular (LV) dysfunction remains a major global health challenge, with inflammation driving its progression under chronic pressure overload, such as hypertension. This study explored the role of interleukin-22 (IL-22), a cytokine associated with tissue protection, in HF induced by transverse aortic constriction (TAC). IL-22 knockout (KO) mice exhibited exacerbated HF, marked by worsened LV hypertrophy, heightened inflammation, and impaired cardiac function compared to wild-type controls. Conversely, treatment with recombinant IL-22Fc improved LV function, reduced inflammatory cell infiltration, and alleviated cardiac remodeling and inflammation. These findings demonstrate that IL-22 plays a critical role in regulating inflammation and cardiac remodeling in pressure overload-induced HF. Targeting IL-22 may represent a promising therapeutic strategy to alleviate HF progression and associated pulmonary complications.

Indexed as

Anti-Inflammatory AgentsHeart FailureHypertrophy, Left VentricularInterleukinsVentricular Dysfunction, LeftVentricular Function, LeftVentricular RemodelingAnimalsDisease Models, AnimalInflammation MediatorsInterleukin-22MaleMice, Inbred C57BLMice, KnockoutSignal TransductionAnti-Inflammatory AgentsInflammation MediatorsInterleukin-22InterleukinsFibrosisHeart FailureInflammationInterleukin-22Transverse aortic constricition

Identifiers

PMID40195212

What Socratic holds

Textmetadata
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 Socratic graph.