Evidence map›Paper›PMID 36988541›Full record

ArticleAging2023

P53/miR-34a/SIRT1 positive feedback loop regulates the termination of liver regeneration.

Junhua Gong, Minghua Cong, Hao Wu, Menghao Wang, He Bai, Jingyuan Wang, Keting Que, Kaiwen Zheng, Wenfeng Zhang, Xiaoli Yang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Involvement of SIRT1-mediated aging in liver diseases.Frontiers in cell and developmental biology · 2025
    Review
  9. 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

14 authors at 9 institutions in 1 country.

Junhua GongDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Minghua CongComprehensive Oncology Department, National Cancer Center/National Clinical Research Center for Cancer/Chinese Academy of Medical Sciences and Peking Union Medical College, Cancer hospital, Beijing 100021, Beijing, China.
Hao WuDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Menghao WangDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
He BaiDepartment of General Surgery, The First Affiliated Hospital of Xi’an Medical University, Lianhu, Xi’an 710000, Shaanxi Province, China.
Jingyuan WangDepartment of Orthopaetics, Dianjiang People’s Hospital of Chongqing, Chongqing 408300, Chongqing, China.
Keting QueDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Kaiwen ZhengDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Wenfeng ZhangDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Xiaoli YangDepartment of Hepatobiliary Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China.
Jianping GongDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Hanping ShiDepartment of Gastrointestinal Surgery/Clinical Nutrition, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China.
Mingyong MiaoInstitute of BioPharmaceutical Research, Liaocheng University, Liaocheng 252059, China.
Fangchao YuanDepartment of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400000, China.
Dalian Medical University · CNChongqing Medical University · CNAffiliated Hospital of Southwest Medical University · CNCapital Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFirst People's Hospital of Chongqing · CNLiaocheng University · CNSecond Affiliated Hospital of Chongqing Medical University · CNXi'an Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe capacity of the liver to restore its architecture and function assures good prognoses of patients who suffer serious hepatic injury, cancer resection, or living donor liver transplantation. Only a few studies have shed light on the mechanisms involved in the termination stage of LR. Here, we attempt to further verify the role of the p53/miR-34a/SIRT1 positive feedback loop in the termination of liver regeneration and its possible relationship with liver cancer.

methodWe performed partial hepatectomy (PH) in mice transfected with adenovirus (Ade) overexpressing P53 and adenovirus-associated virus (AAV) overexpressing miR-34a. LR was analyzed by liver weight/body weight, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and cell proliferation, and the related cellular signals were investigated. Bile acid (BA) levels during LR were analyzed by metabolomics of bile acids.

resultsWe found that the P53/miR-34a/SIRT1 positive feedback loop was activated in the late phase of LR. Overexpression of P53 or miR-34a terminated LR early and enhanced P53/miR-34a/SIRT1 positive feedback loop expression and its proapoptotic effect. T-β-MCA increased gradually during LR and peaked at 7 days after PH. T-β-MCA inhibited cell proliferation and promoted cell apoptosis via facilitating the P53/miR-34a/SIRT1 positive feedback loop during LR by suppressing FXR/SHP. The P53/miR-34a/SIRT1 positive feedback loop was abolished in HCC patients with P53 mutations.

conclusionsThe P53/miR-34a/SIRT1 positive feedback loop plays an important role in the termination of LR. Our findings showed the molecular and metabolic mechanisms of LR termination and provide a potential therapeutic alternative for treating P53-wild-type HCC patients.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsLiver TransplantationMicroRNAsAnimalsApoptosisFeedbackHumansLiver RegenerationLiving DonorsMiceSirtuin 1Tumor Suppressor Protein p53MicroRNAsSIRT1 protein, humanSirt1 protein, mouseSirtuin 1Tumor Suppressor Protein p53HCCliver regenerationmiR-34aP53SIRT1

Identifiers

PMID36988541
PMCPMC10085612
OpenAlexW4361219225

What Socratic holds

Textmetadata
LicenceCC BY
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.