ArticleScientific reports2018
ACE-inhibition induces a cardioprotective transcriptional response in the metabolic syndrome heart.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Immunomodulation and immunopharmacology in heart failure.Nature reviews. Cardiology · 2024Review
- Heart Failure and Drug Therapies: A Metabolic Review.International journal of molecular sciences · 2022Review
- Tale of two kinases: Protein kinase A and CaWorld journal of diabetes · 2021Review
- Antihypertensive drug treatment and susceptibility to SARS-CoV-2 infection in human PSC-derived cardiomyocytes and primary endothelial cells.Stem cell reports · 2021Article
- Benazepril hydrochloride protects against doxorubicin cardiotoxicity by regulating the PI3K/Akt pathway.Experimental and therapeutic medicine · 2021Article
- Perspectives on the Potential Benefits of Antihypertensive Peptides towards Metabolic Syndrome.International journal of molecular sciences · 2020Review
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Authors and funding
14 authors.
Funding
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Abstract
Cardiovascular disease associated with metabolic syndrome has a high prevalence, but the mechanistic basis of metabolic cardiomyopathy remains poorly understood. We characterised the cardiac transcriptome in a murine metabolic syndrome (MetS) model (LDLR-/-; ob/ob, DKO) relative to the healthy, control heart (C57BL/6, WT) and the transcriptional changes induced by ACE-inhibition in those hearts. RNA-Seq, differential gene expression and transcription factor analysis identified 288 genes differentially expressed between DKO and WT hearts implicating 72 pathways. Hallmarks of metabolic cardiomyopathy were increased activity in integrin-linked kinase signalling, Rho signalling, dendritic cell maturation, production of nitric oxide and reactive oxygen species in macrophages, atherosclerosis, LXR-RXR signalling, cardiac hypertrophy, and acute phase response pathways. ACE-inhibition had a limited effect on gene expression in WT (55 genes, 23 pathways), and a prominent effect in DKO hearts (1143 genes, 104 pathways). In DKO hearts, ACE-I appears to counteract some of the MetS-specific pathways, while also activating cardioprotective mechanisms. We conclude that MetS and control murine hearts have unique transcriptional profiles and exhibit a partially specific transcriptional response to ACE-inhibition.
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