Evidence map›Paper›PMID 41674553›Full record

ArticleBioactive materials2026

Ameliorating post-infarction myocardial fibrosis and cardiac function via ROS-responsive hydrogel-mediated IL-11 antibody delivery.

Ting You, Yong Zhang, Haotao Su, Na Wang, Xinkui Zhang, Sainiwaier Anwaier, Xiang Long, Linjiang Han, Yeting Wu, Jialiang Liang and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioactive materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026
    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

23 authors.

Ting YouSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Yong ZhangSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Haotao SuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Na WangGuangdong Provincial Key Laboratory of Biocomputing, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Xinkui ZhangGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Sainiwaier AnwaierGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Xiang LongGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Linjiang HanGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Yeting WuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Jialiang LiangSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Yanzhen YangSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Changjiang YuSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Zerui ChenSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Jian LiuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.
Tucheng SunSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Huanlei HuangSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Shuoji ZhuSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Nanbo LiuSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Ping ZhuSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Jimei ChenSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Jian ZhuangSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Lu WangSchool of Medicine South China University of Technology, Guangzhou, Guangdong, 510006, China.
Xinjian YanGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, 510100, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial fibrosis, driven by fibroblast activation following myocardial infarction (MI), represents a significant pathological process contributing to heart failure progression. Interleukin-11 (IL-11) is recognized as a key mediator in fibrotic pathologies across multiple organs, including the heart. This study demonstrates consistent and specific upregulation of IL-11 expression in a mouse MI model. A single intrapericardial injection of the IL-11-blocking antibody hIL-11 MAB resulted in a modest attenuation of post-MI fibrosis. Subsequently, encapsulation of hIL-11 MAB within reactive oxygen species (ROS)-sensitive hydrogels significantly prolonged drug retention at the injury site, leading to markedly improved therapeutic efficacy. Hydrogel-delivered hIL-11 MAB effectively preserved cardiac structure and function by reducing scar fibrosis, specifically decreasing scar thickness and marginal zone area. IL-11 blockade mediated reduced collagen deposition and enhanced left ventricular contractility, concomitant with a decrease in fibrotic tissue stiffness. These findings provide compelling evidence supporting IL-11 as a therapeutic target for myocardial fibrosis and highlight a novel delivery strategy for developing improved anti-fibrotic interventions.

Indexed as

IL-11Myocardial fibrosisROSSensitive hydrogel

Identifiers

PMID41674553
PMCPMC12887659

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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 OpenQuestion graph.