2021
DOI: 10.1016/j.cardfail.2021.04.003
|View full text |Cite
|
Sign up to set email alerts
|

Cardiac Thyrotropin-releasing Hormone Inhibition Improves Ventricular Function and Reduces Hypertrophy and Fibrosis After Myocardial Infarction in Rats

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

0
2
0

Year Published

2021
2021
2024
2024

Publication Types

Select...
3
1

Relationship

0
4

Authors

Journals

citations
Cited by 4 publications
(2 citation statements)
references
References 34 publications
0
2
0
Order By: Relevance
“…TRH is a cardiac hormone that has important functions in heart regulation and the responses to cardiac stress. It is induced after myocardial infarction and serves as a positive inotrope increasing cardiac contractility and output, but long-term activation can lead to a hypertrophic phenotype in the heart [42][43][44][45] . To further interpret the gene expression data and enhance the GO analysis, a hallmark gene set analysis was conducted with female-derived hiPSC-CMs as a reference.…”
Section: Gene Ontology Pathways Enrichment Reveals Sex Differences In...mentioning
confidence: 99%
“…TRH is a cardiac hormone that has important functions in heart regulation and the responses to cardiac stress. It is induced after myocardial infarction and serves as a positive inotrope increasing cardiac contractility and output, but long-term activation can lead to a hypertrophic phenotype in the heart [42][43][44][45] . To further interpret the gene expression data and enhance the GO analysis, a hallmark gene set analysis was conducted with female-derived hiPSC-CMs as a reference.…”
Section: Gene Ontology Pathways Enrichment Reveals Sex Differences In...mentioning
confidence: 99%
“…Following, we summarize the recent studies about amino acids and nucleotides. The inhibition of cardiac thyrotropin-releasing hormone reduces post-infarct hypertrophy and fibrosis ( Schuman et al, 2021 ). Additionally, triiodothyronine pretreatment improves post-MI dysfunction and inhibits fibrosis by activating the insulin-like growth factor-1/PI3K/Akt signaling pathway ( Zeng et al, 2021 ).…”
Section: Interventions For Cardiac Fibrosismentioning
confidence: 99%