Evidence map›Paper›PMID 30323296›Full record

ArticleCell death & disease2018

PARP1 promote autophagy in cardiomyocytes via modulating FoxO3a transcription.

Cheng Wang, Wenjing Xu, Yanqing Zhang, Fengxiao Zhang, Kai Huang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.0field-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

38 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Autophagy-NADFrontiers in molecular biosciences · 2025
    Review
  9. Review
  10. PARP1 Promotes Heart Regeneration and Cardiomyocyte Proliferation.International journal of biological sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Autophagy induction promoted by mNature communications · 2022
    Article
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Cheng WangClinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Wenjing XuClinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yanqing ZhangClinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fengxiao ZhangClinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. xiaoyou_321@foxmail.com.
Kai HuangClinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. huangkaiunion@gmail.com.
Union Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a key regulatory process in maintaining cellular homoeostasis via lysosome degradation. Growing evidence reveals that poly(ADP-ribose) polymerase-1 (PARP1) is involved in the progression of many cardiovascular diseases. This study was undertaken to discuss the role of PARP1 in cardiomyocyte autophagy. Our results demonstrated that PARP1 was activated in response to starvation-induced myocardial autophagy. We identified Forkhead box O (FoxO)3a as a substrate of PARP1. Upon PARP1 activation, poly(ADP-ribosyl)ation dissociated histone H1 from FoxO3a target gene promoter and promoted FoxO3a nuclear accumulation and binding activity to the target promoters, resulting in increased expression of autophagy related genes. Activated autophagy by PARP1 impaired mitochondrial metabolism and promoted cardiomyocyte death. And PARP1 silencing or specific inhibitors alleviated the promotion of FoxO3 activity upon starvation or myocardial ischemia, thus suppressing cardiac apoptosis and fibrosis. Together, these data indicate that PARP1-mediated poly(ADP-ribosyl)ation of FoxO3a plays a key role in cardiomyocyte autophagy. The utilization of PARP1 as a therapeutic target for related cardiovascular diseases would be desirable.

Indexed as

Adenosine TriphosphateAnimalsAnimals, NewbornAutophagyDisease Models, AnimalForkhead Box Protein O3Gene Expression RegulationHistonesMaleMice, Inbred C57BLMitochondriaMyocardial IschemiaMyocytes, CardiacOxidative PhosphorylationPoly (ADP-Ribose) Polymerase-1Primary Cell CultureAdenosine TriphosphateForkhead Box Protein O3FOXO3 protein, ratHistonesParp1 protein, ratPoly (ADP-Ribose) Polymerase-1RNA, Small Interfering

Identifiers

PMID30323296
PMCPMC6189197
OpenAlexW2897979337

What OpenQuestion 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 OpenQuestion graph.