Evidence map›Paper›PMID 38261867›Full record

ArticleActa pharmaceutica Sinica. B2024

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure.

Jiawen Zhou, Xinyue Sun, Xuelian Chen, Huimin Liu, Xiulian Miao, Yan Guo, Zhiwen Fan, Jie Li, Yong Xu, Zilong Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2024. 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. P2YActa pharmaceutica Sinica. B · 2025
    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

10 authors.

Jiawen ZhouState Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 211198, China.
Xinyue SunState Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 211198, China.
Xuelian ChenState Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 211198, China.
Huimin LiuState Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 211198, China.
Xiulian MiaoInstitute of Biomedical Research, Liaocheng University, Liaocheng 252200, China.
Yan GuoInstitute of Biomedical Research, Liaocheng University, Liaocheng 252200, China.
Zhiwen FanDepartment of Pathology, Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China.
Jie LiDepartment of Infectious Diseases, Nanjing Drum Tower Hospital Affiliated with Nanjing University Medical School, Nanjing 210008, China.
Yong XuState Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 211198, China.
Zilong LiState Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 211198, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver regeneration following injury aids the restoration of liver mass and the recovery of liver function. In the present study we investigated the contribution of megakaryocytic leukemia 1 (MKL1), a transcriptional modulator, to liver regeneration. We report that both MKL1 expression and its nuclear translocation correlated with hepatocyte proliferation in cell and animal models of liver regeneration and in liver failure patients. Mice with MKL1 deletion exhibited defective regenerative response in the liver. Transcriptomic analysis revealed that MKL1 interacted with E2F1 to program pro-regenerative transcription. MAPKAPK2 mediated phosphorylation primed MKL1 for its interaction with E2F1. Of interest, phospholipase d2 promoted MKL1 nuclear accumulation and liver regeneration by catalyzing production of phosphatidic acid (PA). PA administration stimulated hepatocyte proliferation and enhanced survival in a MKL1-dependent manner in a pre-clinical model of liver failure. Finally, PA levels was detected to be positively correlated with expression of pro-regenerative genes and inversely correlated with liver injury in liver failure patients. In conclusion, our data reveal a novel mechanism whereby MKL1 contributes to liver regeneration. Screening for small-molecule compounds boosting MKL1 activity may be considered as a reasonable approach to treat acute liver failure.

Indexed as

HepatocytesLiver failureLiver regenerationPhosphatidic acidPhospholipase d2Transcription factorTranscription regulationTranslational medicine

Identifiers

PMID38261867
PMCPMC10793099

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.