ArticleMolecular medicine reports2017
Renal sympathetic denervation alleviates myocardial fibrosis following isoproterenol-induced heart failure.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Cardiorenal Associations in Preclinical Modeling: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2026Pooled it
- Pleiotropic effects of renal denervation beyond blood pressure reduction.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Renal Denervation in Heart Failure Treatment: Data for a Self-Fulfilling Prophecy.Journal of clinical medicine · 2024Review
- The role of afferent renal nerves in regulating sympathetic outflow via central nervous system mechanisms.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
- Naringin attenuates rat myocardial ischemia/reperfusion injury via PI3K/Akt pathway-mediated inhibition of apoptosis, oxidative stress and autophagy.Experimental and therapeutic medicine · 2021Article
- Diosmetin exerts cardioprotective effect on myocardial ischaemia injury in neonatal rats by decreasing oxidative stress and myocardial apoptosis.Clinical and experimental pharmacology & physiology · 2020Article
- Perindopril Improves Cardiac Function by Enhancing the Expression of SIRT3 and PGC-1α in a Rat Model of Isoproterenol-Induced Cardiomyopathy.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to determine if renal sympathetic denervation (RSD) may alleviate isoproterenol-induced left ventricle remodeling, and to identify the underlying mechanism. A total of 70 rats were randomly divided into control (n=15), sham operation (n=15), heart failure (HF) with sham operation (HF + sham; n=20) and HF with treatment (HF + RSD; n=20) groups. The HF model was established by subcutaneous injection of isoproterenol; six weeks later, 1eft ventricular internal diameter at end‑systole (LVIDs), left ventricular systolic posterior wall thickness (LVPWs), 1eft ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured. Plasma norepinephrine (NE), angiotensin II (Ang II) and aldosterone (ALD) levels were measured by ELISA. Myocardial collagen volume fraction (CVF) was determined by Masson's staining. Reverse transcription‑quantitative polymerase chain reaction was used to determine the mRNA expression levels of ventricular transforming growth factor‑β (TGF‑β), connective tissue growth factor (CTGF) and microRNAs (miRs), including miR‑29b, miR‑30c and miR‑133a. The results demonstrated that LVIDs and LVPWs in the HF + RSD group were significantly decreased compared with the HF + sham group. By contrast, LVFS and LVEF in the HF + RSD group were significantly increased compared with the HF + sham group. RSD significantly reduced the levels of plasma NE, Ang II and ALD. CVF in the HF + RSD group was reduced by 38.1% compared with the HF + sham group. Expression levels of TGF‑β and CTGF were decreased, whereas those of miR‑29b, miR‑30c and miR‑133a were increased, in the HF + RSD group compared with the HF + sham group. These results indicated that RSD alleviates isoproterenol‑induced left ventricle remodeling potentially via downregulation of TGF‑β/CTGF and upregulation of miR‑29b, miR‑30c and miR‑133a. RSD may therefore be an effective non‑drug therapy for the treatment of heart failure.
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Registered trials
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