Evidence map›Paper›PMID 34305596›Full record

ArticleFrontiers in pharmacology2021

Ectopic Overexpression of PPARγ2 in the Heart Determines Differences in Hypertrophic Cardiomyopathy After Treatment With Different Thiazolidinediones in a Mouse Model of Diabetes.

Xuemei Cao, Min Mao, Junlin Diao, Yi Hou, Hong Su, Yongjun Gan, Jibin Li, Xiaoyong Tong, Chaodong Wu, Zhong Zuo and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
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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

11 authors at 5 institutions in 2 countries.

Xuemei CaoDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Min MaoThe Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Junlin DiaoDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yi HouThe Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hong SuThe Chongqing Key Laboratory of Translational Medicine in Major Metabolic Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yongjun GanExperimental Teaching & Management Center, Chongqing Medical University, Chongqing, China.
Jibin LiDepartment of Nutrition and Food Hygiene, School of Public Health and Management, Chongqing Medical University, Chongqing, China.
Xiaoyong TongSchool of Pharmaceutical Sciences, Chongqing University, Chongqing, China.
Chaodong WuDepartment of Nutrition and Food Science, Texas A&M University, College Station, TX, United States.
Zhong ZuoDepartment of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xiaoqiu XiaoDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNChongqing Public Health Medical Center · CNChongqing University · CNTexas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical controversy of rosiglitazone as a hypoglycemic agent is potentially associated with heart failure, mainly due to its potent activation of peroxisome proliferator-activated receptor γ (PPARγ). PPARγ partial agonists showed superior pharmacological profiles to rosiglitazone. This study compared differences in cardiac morphology and function of the PPARγ partial agonist CMHX008 with rosiglitazone. High-fat diet (HFD) induced obese mice, ob/ob mice and cardiomyocytes overexpressing PPARγ2 were treated with CMHX008 or rosiglitazone. Heart function, myocardial morphology, and hypertrophy-related gene expression were examined. Clinical information from patients with type 2 diabetes mellitus (T2DM) who had taken rosiglitazone and undergone Doppler echocardiography was collected. HFD and ob/ob mice significantly developed cardiac contractile dysfunction, with upregulated PPARγ2 protein levels in heart tissues. Cardiomyocytes of HFD and ob/ob mice were disorderly arranged, the cell areas expanded, and collagen accumulated.

Indexed as

cardiac hypertrophydiabetic cardiomyopathyinsulin sensitizersPPARγrosiglitazone

Identifiers

PMID34305596
PMCPMC8293689
OpenAlexW3181418139

What Socratic 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 Socratic graph.