Evidence map›Paper›PMID 33025271›Full record

ArticleJournal of cardiovascular translational research2021

AdipoRon Attenuates Hypertension-Induced Epithelial-Mesenchymal Transition and Renal Fibrosis via Promoting Epithelial Autophagy.

Yan Li, Bei Song, Chengchao Ruan, WenJie Xue, Jianrong Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Efficacy of ADIPOR1 and ADIPOR2 peptide-agonist AdipoRon in preventing contracture in a rabbit model of arthrofibrosis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Mitophagy in hypertension-mediated organ damage.Frontiers in cardiovascular medicine · 2023
    Review
  16. Article
  17. Role of adiponectin in osteoarthritis.Frontiers in cell and developmental biology · 2022
    Review
  18. Article
  19. Article
  20. Frontiers in pharmacology · 2021
    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

5 authors at 2 institutions in 1 country.

Yan Li *Department of Cardiology, RuiJin Hospital/LuWan Branch, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Bei Song *Department of General Practice, RuiJin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Chengchao RuanState Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
WenJie XueHuangpu District Bansongyuan Road Health Service Center, Shanghai, China. 290578605@qq.com.
Jianrong ZhaoDepartment of Cardiology, RuiJin Hospital/LuWan Branch, School of Medicine, Shanghai Jiaotong University, Shanghai, China. drzjr@126.com.
Ruijin Hospital · CNShanghai Huangpu District Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension-induced epithelial-mesenchymal transition (EMT) is a major mechanism of renal fibrosis. Adiponectin protects against hypertension-induced target organ damage. AdipoRon is an orally active synthetic adiponectin receptor agonist. However, it is unclear whether AdipoRon could attenuate EMT and renal fibrosis in hypertensive mice. C57BJ/6J mice were utilized to induce DOCA-salt-sensitive hypertensive model. Hypertension results in an altered adiponectin expression and promotes EMT in the kidney. In vitro, AdipoRon inhibits aldosterone (Aldo)-induced EMT and promotes autophagic flux in HK-2 epithelial cells. Mechanically, AdipoRon activates AMPK/ULK1 pathway in epithelial cells. Blockade of AMPK activation, as well as inhibition of autophagy, blocks the effects of AdipoRon on Aldo-induced EMT. Moreover, AdipoRon treatment promotes autophagy and improves renal fibrosis in DOCA-salt-hypertensive mice. Our data suggest that AdipoRon could be a potential therapeutic option to prevent renal fibrosis in hypertensive patients. Graphical abstract.

Indexed as

AMP-Activated Protein KinasesAnimalsAutophagyAutophagy-Related Protein-1 HomologCell LineDisease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFibrosisHumansHypertensionIntracellular Signaling Peptides and ProteinsKidneyKidney DiseasesMiceMice, Inbred C57BLAdipoRonAMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsPiperidinesULK1 protein, humanAdipoRonAutophagyEpithelial-mesenchymal transitionHypertensionRenal fibrosis

Identifiers

PMID33025271
OpenAlexW3092471612

What OpenQuestion holds

Textmetadata
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.