Serum microRNA-30d is a sensitive biomarker for angiotensin II-induced cardiovascular complications in rats

Miyamoto, Masaki; Ono, Katsushige

doi:10.1007/s00380-021-01853-8

Cited by 2 publications

(1 citation statement)

References 35 publications

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“…Few papers reported that miR-30d was increased, such as Morishima et al found miR-30d was increased in the atrium and serum of Ang II‑induced cardiovascular complications in rats. 32 Instead, most of the studies showed that miR-30d was down-regulated trigged by adverse cardiac remodeling, such as in heart samples of chronic kidney disease (CKD)-induced left ventricular hypertrophy (LVH) mice model and in serum samples of dogs with eccentric or concentric cardiac hypertrophy induced by myxomatous mitral valve degeneration (MMVD) or pulmonic stenosis (PS). 33 , 34 Moreover, the in vivo role of miR-30d in cardiac remodeling was explored in some studies.…”

Section: Discussionmentioning

confidence: 99%

Targeting miR-30d reverses pathological cardiac hypertrophy

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Targeting miR-30d reverses pathological cardiac hypertrophy

et al. 2022

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Plasma and Myocardial miRNomes Similarities and Differences during Cardiac Remodelling and Reverse Remodelling in a Murine Model of Heart Failure with Preserved Ejection Fraction

Thibodeau,

Labbé,

Walsh-Wilkinson

et al. 2024

Biomolecules

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Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome characterised by multiple risk factors touching various organs outside the heart. Using a murine HFpEF model, we studied cardiac reverse remodelling (RR) after stopping the causing metabolic-hypertensive stress (MHS; Angiotensin II [AngII] and a high-fat diet [HFD]) after 28 days and introducing voluntary exercise (VE) for four more weeks. We measured the effects of MHS and RR on the plasma and myocardial microRNA (miR) profile (miRNome) to characterise better cardiac and non-cardiac responses to HFpEF-inducing risk factors and their reversibility. AngII alone, the HFD or the MHS caused cardiac hypertrophy (CH), left ventricular (LV) concentric remodelling and left atrial enlargement in females. Only AngII and the MHS, but not HFD, did in males. After RR, CH, LV concentric remodelling and atrial enlargement were normalised. Among the 25 most abundant circulating miRs, 10 were modulated by MHS. Plasma miRNomes from AngII, HFD or MHS mice shared 31 common significantly modulated miRs (24 upregulated and 7 downregulated), suggesting that the response of organs producing the bulk of those circulating miRs was similar even for seemingly different stress. In the LV, 19 out of 25 most expressed miRs were modulated. RR restored normality for the plasma miRNome but not for the LV miRNome, which remained mostly unchanged. Our results suggest that abnormalities persist in the myocardium of the HFpEF mice and that the normalisation of circulatory markers may be falsely reassuring after recovery.

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Serum microRNA-30d is a sensitive biomarker for angiotensin II-induced cardiovascular complications in rats

Cited by 2 publications

References 35 publications

Targeting miR-30d reverses pathological cardiac hypertrophy

Targeting miR-30d reverses pathological cardiac hypertrophy

Plasma and Myocardial miRNomes Similarities and Differences during Cardiac Remodelling and Reverse Remodelling in a Murine Model of Heart Failure with Preserved Ejection Fraction

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