MicroRNA-30 regulates left ventricular hypertrophy in chronic kidney disease.
Cardiology
Cardiovascular disease
Chronic kidney disease
Nephrology
Journal
JCI insight
ISSN: 2379-3708
Titre abrégé: JCI Insight
Pays: United States
ID NLM: 101676073
Informations de publication
Date de publication:
24 05 2021
24 05 2021
Historique:
received:
17
03
2020
accepted:
07
04
2021
pubmed:
14
4
2021
medline:
15
2
2022
entrez:
13
4
2021
Statut:
epublish
Résumé
Left ventricular hypertrophy (LVH) is a primary feature of cardiovascular complications in patients with chronic kidney disease (CKD). miRNA-30 is an important posttranscriptional regulator of LVH, but it is unknown whether miRNA-30 participates in the process of CKD-induced LVH. In the present study, we found that CKD not only resulted in LVH but also suppressed miRNA-30 expression in the myocardium. Rescue of cardiomyocyte-specific miRNA-30 attenuated LVH in CKD rats without altering CKD progression. Importantly, in vivo and in vitro knockdown of miRNA-30 in cardiomyocytes led to cardiomyocyte hypertrophy by upregulating the calcineurin signaling directly. Furthermore, CKD-related detrimental factors, such as fibroblast growth factor-23, uremic toxin, angiotensin II, and transforming growth factor-β, suppressed cardiac miRNA-30 expression, while miRNA-30 supplementation blunted cardiomyocyte hypertrophy induced by such factors. These results uncover a potentially novel mechanism of CKD-induced LVH and provide a potential therapeutic target for CKD patients with LVH.
Identifiants
pubmed: 33848263
pii: 138027
doi: 10.1172/jci.insight.138027
pmc: PMC8262338
doi:
pii:
Substances chimiques
MIRN30 microRNA, rat
0
MicroRNAs
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
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