Evidence map›Paper›PMID 34328199›Full record

ArticleMolecular medicine reports2021

Liquiritigenin attenuates isoprenaline‑induced myocardial fibrosis in mice through the TGF‑β1/Smad2 and AKT/ERK signaling pathways.

Li Li, Hui Fang, Yong-Hong Yu, Shan-Xin Liu, Zhi-Qiang Yang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Exploring Mechanistic Targets ofInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Polygonatum sibiricum component liquiritigenin restrains breast cancer cell invasion and migration by inhibiting HSP90 and chaperone-mediated autophagy.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. 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.

Li LiDepartment of Ultrasonography, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang 310012, P.R. China.
Hui FangDepartment of Ultrasonography, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang 310012, P.R. China.
Yong-Hong YuDepartment of Ultrasonography, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang 310012, P.R. China.
Shan-Xin LiuDepartment of Cardiology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang 310000, P.R. China.
Zhi-Qiang YangType‑B Ultrasonic Room, Heart Center, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang 310000, P.R. China.
Tongde Hospital of Zhejiang Province · CNAffiliated Hospital of Hangzhou Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial fibrosis is a pathological process characterized by excessive accumulation of extracellular matrix in myocardial interstitial spaces. Myocardial fibrosis is a fundamental process in ventricular remodeling and a primary contributor to the progression of heart failure. Liquiritigenin (LQ) is a flavanone compound with anti‑oxidative, anti‑carcinogenic, anti‑inflammatory and estrogenic properties. The present study aimed to investigate the regulatory potential of LQ treatment in a mouse model of isoprenaline (ISO)‑induced cardiac fibrosis and in cultured H9C2 cardiomyocytes stimulated with angiotensin II (Ang II). The treatment of ISO‑induced mice with LQ significantly decreased the levels of cardiac injury‑related proteins in the serum and ECM accumulation in mouse heart tissues. LQ treatment also effectively alleviated cardiac dysfunction in ISO‑treated mice. Further analyses revealed that LQ inhibited ISO‑induced collagen formation and activation of the transforming growth factor‑β1 (TGF‑β1)/Smad2 and protein kinase B (AKT)/extracellular signal‑regulated kinase (ERK) signaling pathways. As a major pathological event in myocardial fibrosis, the apoptosis of cardiomyocytes has been considered a key mechanism contributing to impaired left ventricle performance. The pretreatment of rat cardiomyocytes with LQ significantly reduced the apoptosis of H9C2 cells, and inhibited Ang II‑induced activation of the TGF‑β1/Smad2 and AKT/ERK pathways. In conclusion, the present study revealed that LQ ameliorated ISO‑induced myocardial fibrosis in mice and inhibited the apoptosis of cardiomyocytes

Indexed as

Angiotensin IIAnimalsApoptosisCell LineExtracellular Signal-Regulated MAP KinasesFibrosisFlavanonesHeart DiseasesHeart Function TestsIsoproterenolMaleMiceMice, Inbred C57BLMyocytes, CardiacProto-Oncogene Proteins c-aktRatsAngiotensin IIExtracellular Signal-Regulated MAP KinasesFlavanonesIsoproterenolliquiritigeninProto-Oncogene Proteins c-aktSmad2 ProteinSmad2 protein, mouseSmad2 protein, ratTgfb1 protein, mouseTgfb1 protein, ratTransforming Growth Factor beta1extracellular signal‑regulated kinaseliquiritigeninmyocardial fibrosisprotein kinase BSmad2transforming growth factor β1ultrasound imaging

Identifiers

PMID34328199
PMCPMC8365605
OpenAlexW3185508817

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.