Evidence map›Paper›PMID 29101624›Full record

ArticleHerz2019

Genistein attenuates pathological cardiac hypertrophy in vivo and in vitro.

Y Meng, Y Zhang, Z Ma, H Zhou, J Ni, H Liao, Q Tang

Abstract read
PubMed Publisher
In one paragraph

Article in Herz, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

5 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Pharmacological Effects of Genistein on Cardiovascular Diseases.Evidence-based complementary and alternative medicine : eCAM · 2023
    Review
  4. Review
  5. 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

7 authors at 4 institutions in 1 country.

Y MengDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China.
Y ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China.
Z MaDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China.
H ZhouDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China.
J NiDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China.
H LiaoDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China.
Q TangDepartment of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, 430060, Wuhan, Hubei, China. qztang@whu.edu.cn.
Renmin Hospital of Wuhan University · CNWuhan Business University · CNWuhan University · CNHubei University · CN

Funding

National Natural Science Foundation of China (CN) 81270303 and 81470516
6 · The paper itself

Abstract

backgroundWe investigated the effects and underlying mechanisms of genistein on pathological cardiac hypertrophy in vivo and in vitro. MATERIALS AND

methodsA cardiac hypertrophy model was developed by aortic banding (AB). C57/BL6 mice were randomly assigned to sham + vehicle (CON), sham + genistein (GEN), AB + vehicle (AB), and AB + genistein groups. Genistein (40 mg/kg/day) was administered by gavage for 7 weeks. After assessing the echocardiographic and hemodynamic parameters, mouse hearts were harvested for histopathological and molecular biological analysis. In the in vitro experiments, neonatal rat cardiomyocytes (NRCM) were prepared to test whether genistein could prevent cardiomyocyte hypertrophy induced by phenylephrine (PE).

resultsCompared with the CON or GEN group, mice in the AB group exhibited a markedly increased cross-sectional area of cardiomyocytes, collagen volume fraction, and up-regulated expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), beta-myosin heavy chain (β-MHC) promoter, connective tissue growth factor (CTGF), collagen Iα, collagen III, fibronectin, transforming growth factor (TGF)-β1, and vimentin mRNA, as well as down-regulated expression of SERCA2α and α‑MHC mRNA. Genistein significantly attenuated the expression of these abnormal hypertrophic and fibrotic markers. This anti-hypertrophic effect might be associated with the inhibition of MAPK (ERK1/2, P38, and JNK1/2) and AKT/GSK-3β signaling. However, in the in vitro experiment, genistein only inhibited hyperphosphorylation of JNK1/2 in the early stage of prohypertrophic stimulation. Genistein could not attenuate PE-induced cardiomyocyte hypertrophy even after pretreatment with sp61005 (a selective inhibitor of JNK1/2).

conclusionGenistein attenuated pressure overload-induced cardiac hypertrophy in vivo and PE induced NRCM hypertrophy in vitro. The underlying mechanisms of genistein activity may be associated with blocking the JNK1/2 signaling pathways.

Indexed as

CardiomegalyGenisteinProtein Kinase InhibitorsAnimalsGlycogen Synthase Kinase 3 betaMiceMice, Inbred C57BLMyocytes, CardiacRandom AllocationGenisteinGlycogen Synthase Kinase 3 betaProtein Kinase InhibitorsCardiomegalyEndomyocardial fibrosisJNK1/2 kinaseMitogen-activated protein kinase phosphataseProtein kinase inhibitors

Identifiers

PMID29101624
OpenAlexW2766366628

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.