Evidence map›Paper›PMID 31767630›Full record

ArticleGut2020

Growth differentiation factor 11 attenuates liver fibrosis via expansion of liver progenitor cells.

Zhen Dai, Guangqi Song, Asha Balakrishnan, Taihua Yang, Qinggong Yuan, Selina Möbus, Anna-Carina Weiss, Martin Bentler, Jimin Zhu, Xuemei Jiang and 11 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Gut, 2020. 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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  6. Stem cell-based therapeutic strategies for liver aging.Liver research (Beijing, China) · 2025
    Review
  7. Article
  8. Review
  9. Periplakin Attenuates Liver Fibrosis via Reprogramming CD44Cellular and molecular gastroenterology and hepatology · 2025
    Article
  10. Review
  11. Article
  12. GDF11: An emerging therapeutic target for liver diseases and fibrosis.Journal of cellular and molecular medicine · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 3 institutions in 2 countries.

Zhen DaiDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Guangqi SongResearch Group MicroRNA in Liver Regeneration, Cluster of Excellence REBIRTH, Hannover Medical School, Hannover, Germany.
Asha BalakrishnanDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Taihua YangDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Qinggong YuanDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Selina MöbusDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Anna-Carina WeissInstitute for Molecular Biology, Hannover Medical School, Hannover, Germany.
Martin BentlerInstitute of Experimental Hematology, Hannover Medical School, Hannover, Germany.
Jimin ZhuDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.ORCID 0000-0002-2150-473X
Xuemei JiangDepartment of Gastroenterology, Central South University Xiangya School of Medicine Affiliated Haikou Hospital, Haikou, China.
Xizhong ShenDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Heike BantelDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Elmar JaeckelDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Andreas KispertInstitute for Molecular Biology, Hannover Medical School, Hannover, Germany.
Arndt VogelDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Anna SaborowskiDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Hildegard BüningInstitute of Experimental Hematology, Hannover Medical School, Hannover, Germany.
Michael MannsDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Tobias CantzDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Michael OttDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany sharma.amar@mh-hannover.de ott.michael@mh-hannover.de.
Amar Deep SharmaDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany sharma.amar@mh-hannover.de ott.michael@mh-hannover.de.ORCID 0000-0003-3599-2372
Medizinische Hochschule Hannover · DEFudan University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLiver fibrosis and cirrhosis resulting from chronic liver injury represent a major healthcare burden worldwide. Growth differentiation factor (GDF) 11 has been recently investigated for its role in rejuvenation of ageing organs, but its role in chronic liver diseases has remained unknown. Here, we investigated the expression and function of GDF11 in liver fibrosis, a common feature of most chronic liver diseases.

designWe analysed the expression of GDF11 in patients with liver fibrosis, in a mouse model of liver fibrosis and in hepatic stellate cells (HSCs) as well as in other liver cell types. The functional relevance of GDF11 in toxin-induced and cholestasis-induced mouse models of liver fibrosis was examined by in vivo modulation of

resultsWe showed that the expression of GDF11 is upregulated in patients with liver fibrosis and in experimentally induced murine liver fibrosis models. Furthermore, we found that therapeutic application of GDF11 mounts a protective response against fibrosis by increasing the number of LGR5+ progenitor cells in the liver.

conclusionCollectively, our findings uncover a protective role of GDF11 during liver fibrosis and suggest a potential application of GDF11 for the treatment of chronic liver disease.

Indexed as

AnimalsBone Morphogenetic ProteinsDisease Models, AnimalFluorescent Antibody TechniqueGene FlowGrowth Differentiation FactorsHumansIn Situ HybridizationLiverLiver CirrhosisMaleMiceMice, Inbred BALB CStem CellsUp-RegulationBone Morphogenetic ProteinsGDF11 protein, humanGdf11 protein, mouseGrowth Differentiation Factorschronic liver diseasefibrosisGDF11 and LGR5hepatic stellate cellsmyofibroblastsstem cells

Identifiers

PMID31767630
PMCPMC7282557
OpenAlexW2989567859

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.