Evidence map›Paper›PMID 42793141›Full record

ReviewBiomolecules2026

Interleukin-11 Signaling in Liver Disease: Mechanisms, Cellular Crosstalk, and Therapeutic Potential.

Zhiyuan Chen, Fan Yu, Yanhua Qiu, Jun Lin, Meilian Yu, Jinwei Yan, Xianzhi Liu

Abstract readReview
In one paragraph

Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Zhiyuan ChenDepartment of Gastroenterology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361000, China.
Fan YuDepartment of Gastrointestinal Surgery, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361000, China.
Yanhua QiuDepartment of Anesthesiology, West China Hospital of Sichuan University, Chengdu 610041, China.
Jun LinDepartment of Pediatrics, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361000, China.
Meilian YuDepartment of Gastroenterology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361000, China.
Jinwei YanDepartment of Anesthesiology, West China Hospital of Sichuan University, Chengdu 610041, China.
Xianzhi LiuDepartment of Gastroenterology, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361000, China.

Funding

Foundation for Cultivated Young Talents of Fujian Province, China 2025350237Fujian Provincial Health and Technology Program - Young and Middle-aged Key Talent Development Project 2025GGA095National Natural Science Foundation of China 82500759Natural Science Foundation of Fujian Province 2026D019Postdoctoral Fellowship Program of CPSF 2025M772140Postdoctoral Fellowship Program of CPSF GZB20240394Xiamen Health High Quality Development Project 2024GZL-GG06Young Investigator Research Program of Xiang'an Hospital of Xiamen University XAH24007
6 · The paper itself

Abstract

The liver has a remarkable regenerative capacity, but persistent injury caused by drugs, metabolic dysfunction, alcohol, and chronic inflammation can overwhelm this process and promote fibrosis and hepatocellular carcinoma. Interleukin-11 (IL-11), a cytokine that signals through glycoprotein 130 (gp130), was historically considered hepatoprotective; however, accumulating experimental evidence predominantly identifies endogenous IL-11 as an amplifier of liver injury and maladaptive repair. In hepatocytes, IL-11 promotes oxidative stress, mitochondrial dysfunction, and cell death while limiting effective regeneration. In hepatic stellate cells, it sustains myofibroblastic activation and extracellular matrix production, while crosstalk with hepatocytes, macrophages, and the matrix reinforces a fibroinflammatory niche. In hepatocellular carcinoma, experimental and associative clinical evidence implicates IL-11 in tumor growth, invasion, metastatic colonization, postoperative recurrence, stromal remodeling, and immune suppression. These findings have supported the development of therapeutic strategies targeting the IL-11/IL-11RA axis, with the potential to provide broad therapeutic benefits across a wide spectrum of liver diseases. This review summarizes IL-11 regulation and signaling in liver disease; discusses its roles in liver injury, fibrosis, and hepatocellular carcinoma; and evaluates the opportunities and challenges of IL-11-targeted therapy.

Indexed as

Interleukin-11Liver DiseasesSignal TransductionAnimalsCarcinoma, HepatocellularHepatic Stellate CellsHumansLiver NeoplasmsIL11 protein, humanInterleukin-11cellular crosstalkinterleukin-11liver diseasetargeted therapy

Identifiers

PMID42793141
PMCPMC13604896

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Registered trials

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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.