Evidence map›Paper›PMID 37985436›Full record

ArticleJournal of cellular and molecular medicine2024

Honokiol ameliorates angiotensin II-induced cardiac hypertrophy by promoting dissociation of the Nur77-LKB1 complex and activating the AMPK pathway.

Xiaoyan Lin, Hailin Zhang, Yong Chu, Yuze Zhang, Changsheng Xu, Hong Xie, Qinyun Ruan, Jinxiu Lin, Chun-Kai Huang, Dajun Chai

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. 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 at 1 institution in 1 country.

Xiaoyan LinEchocardiological Department, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Hailin ZhangCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Yong ChuCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Yuze ZhangCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Changsheng XuCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Hong XieCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Qinyun RuanEchocardiological Department, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Jinxiu LinCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Chun-Kai HuangCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Dajun ChaiCardiovascular Department, Fujian Institute of Hypertension, The First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID 0000-0001-9477-9956
Fujian Medical University · CN

Funding

Fujian Medical University 2020QH2032Fujian Provincial Department of Science and Technology 2018Y9088Fujian Provincial Health Technology Project 2020QNA052Natural Science Foundation of Fujian Province 2020J01962
6 · The paper itself

Abstract

Pathological cardiac hypertrophy is a key contributor to heart failure, and the molecular mechanisms underlying honokiol (HNK)-mediated cardioprotection against this condition remain worth further exploring. This study aims to investigate the effect of HNK on angiotensin II (Ang II)-induced myocardial hypertrophy and elucidate the underlying mechanisms. Sprague-Dawley rats were exposed to Ang II infusion, followed by HNK or vehicle treatment for 4 weeks. Our results showed that HNK treatment protected against Ang II-induced myocardial hypertrophy, fibrosis and dysfunction in vivo and inhibited Ang II-induced hypertrophy in neonatal rat ventricular myocytes in vitro. Mechanistically, HNK suppressed the Ang II-induced Nur77 expression at the transcriptional level and promoted ubiquitination-mediated degradation of Nur77, leading to dissociation of the Nur77-LKB1 complex. This facilitated the translocation of LKB1 into the cytoplasm and activated the LKB1-AMPK pathway. Our findings suggest that HNK attenuates pathological remodelling and cardiac dysfunction induced by Ang II by promoting dissociation of the Nur77-LKB1 complex and subsequent activation of AMPK signalling. This study uncovers a novel role of HNK on the LKB1-AMPK pathway to protect against cardiac hypertrophy.

Indexed as

Allyl CompoundsAMP-Activated Protein KinasesAngiotensin IIBiphenyl CompoundsPhenolsAnimalsCardiomegalyMyocytes, CardiacRatsRats, Sprague-DawleyAllyl CompoundsAMP-Activated Protein KinasesAngiotensin IIBiphenyl CompoundshonokiolPhenolsangiotensin IIcardiac hypertrophyhonokiolLKB1Nur77

Identifiers

PMID37985436
PMCPMC10805491
OpenAlexW4388851093

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.