Evidence map›Paper›PMID 31127082›Full record

ArticleCell death & disease2019

Oridonin protects against cardiac hypertrophy by promoting P21-related autophagy.

Man Xu, Chun-Xia Wan, Si-Hui Huang, Hui-Bo Wang, Di Fan, Hai-Ming Wu, Qing-Qing Wu, Zhen-Guo Ma, Wei Deng, Qi-Zhu Tang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Mechanisms of MCL-1 Protein Stability Induced by MCL-1 Antagonists in B-Cell Malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  17. Article
  18. Article
  19. Review
  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

10 authors at 2 institutions in 1 country.

Man XuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Chun-Xia WanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Si-Hui HuangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Hui-Bo WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Di FanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Hai-Ming WuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Qing-Qing WuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Zhen-Guo MaDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Wei DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. vivideng1982@whu.edu.cn.
Qi-Zhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. qztang@whu.edu.cn.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an endogenous protective process; the loss of autophagy could destabilize proteostasis and elevate intracellular oxidative stress, which is critically involved in the development of cardiac hypertrophy and heart failure. Oridonin, a natural tetracycline diterpenoid from the Chinese herb Rabdosia, has autophagy activation properties. In this study, we tested whether oridonin protects against cardiac hypertrophy in mice and cardiomyocytes. We implemented aortic banding to induce a cardiac hypertrophy mouse model, and oridonin was given by gavage for 4 weeks. Neonatal rat cardiomyocytes were stimulated with angiotensin II to simulate neurohumoural stress. Both in vivo and in vitro studies suggested that oridonin treatment mitigated pressure overload-induced cardiac hypertrophy and fibrosis, and also preserved heart function. Mice that received oridonin exhibited increased antioxidase activities and suppressed oxidative injury compared with the aortic banding group. Moreover, oridonin enhanced myocardial autophagy in pressure-overloaded hearts and angiotensin II-stimulated cardiomyocytes. Mechanistically, we discovered that oridonin administration regulated myocardial P21, and cytoplasmic P21 activated autophagy via regulating Akt and AMPK phosphorylation. These findings were further corroborated in a P21 knockout mouse model. Collectively, pressure overload-induced autophagy dysfunction causes intracellular protein accumulation, resulting in ROS injury while aggravating cardiac hypertrophy. Thus, our data show that oridonin promoted P21-related autophagic lysosomal degradation, hence attenuating oxidative injury and cardiac hypertrophy.

Indexed as

Angiotensin IIAnimalsAntineoplastic Agents, PhytogenicAntioxidantsAutophagyCardiomegalyCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalDiterpenes, KauraneMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacOxidative StressAngiotensin IIAntineoplastic Agents, PhytogenicAntioxidantsCyclin-Dependent Kinase Inhibitor p21Diterpenes, KauraneoridoninProto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID31127082
PMCPMC6534559
OpenAlexW2945870418

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.