MicroRNA‑24 attenuates diabetic vascular remodeling by suppressing the NLRP3/caspase‑1/IL‑1β signaling pathway Corrigendum in /10.3892/ijmm.2022.5079

Fan,Zhixing; Yang,Jian; Yang,Chaojun; Zhang,Jing; Cai,Wanying; Huang,Congxin

doi:10.3892/ijmm.2020.4533

MicroRNA‑24 attenuates diabetic vascular remodeling by suppressing the NLRP3/caspase‑1/IL‑1β signaling pathway

Corrigendum in: /10.3892/ijmm.2022.5079

Authors:
- Zhixing Fan
- Jian Yang
- Chaojun Yang
- Jing Zhang
- Wanying Cai
- Congxin Huang
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Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Cardiology, The People's Hospital of Three Gorges University/The First People's Hospital of Yichang, Yichang, Hubei 443000, P.R. China, Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei 443000, P.R. China
Published online on: March 9, 2020 https://doi.org/10.3892/ijmm.2020.4533
Pages: 1534-1542
Copyright: © Fan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Vascular remodeling plays an important role in the pathogenesis of diabetic cardiovascular complications. Previous published research has indicated that microRNA‑24 (miR‑24) is involved in diabetic vascular remodeling, but the underlying molecular mechanisms have yet to be fully elucidated. The aim of the present study was to investigate whether adenovirus‑mediated miR‑24 overexpression can suppress the NOD‑like receptor family pyrin domain‑containing 3 (NLRP3)‑related inflammatory signaling pathway and attenuate diabetic vascular remodeling. The carotid arteries of diabetic rats were harvested and prepared for analysis. Reverse transcription‑quantitative PCR and western blotting assays were used to detect the expressions of related mRNAs and proteins. Morphological examinations, including hematoxylin and eosin, immunohistochemical and Masson's trichrome staining, were also performed. The results of the present study demonstrated that miR‑24 upregulation suppressed neointimal hyperplasia and accelerated reendothelialization in the injured arteries, lowered the expression of NLRP3, apoptosis‑associated speck‑like protein, caspase‑1, proliferating cell nuclear antigen, CD45, interleukin (IL)‑1β, IL‑18 and tumor necrosis factor‑α, and increased the expression of CD31, smooth muscle (SM) α‑actin and SM‑myosin heavy chain. These data indicated that miR‑24 overexpression can attenuate vascular remodeling in a diabetic rat model through suppressing the NLRP3/caspase‑1/IL‑1β signaling pathway.

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