Revealing Landscape of Competing Endogenous RNA Networks in Sepsis-Induced Cardiovascular Diseases

⁴ Department of Emergency Critical Care, Ziyang People’s Hospital, Ziyang Hospital of Sichuan Provincial People’s Hospital, 641300 Ziyang, Sichuan, China

^*Correspondence: gongjian126@126.com (Jian Gong)

Rev. Cardiovasc. Med. 2023, 24(7), 214; https://doi.org/10.31083/j.rcm2407214

Submitted: 14 November 2022 | Revised: 11 January 2023 | Accepted: 6 February 2023 | Published: 24 July 2023

(This article belongs to the Special Issue Advances with miRNAs in Cardiovascular Disease: miRNA-Based Therapeutic Strategies)

This is an open access article under the CC BY 4.0 license.

Abstract

Cardiovascular dysfunction induced by sepsis is one of the most common phenotypes of cardiovascular diseases (CVDs), which is closely related to the high mortality of sepsis and is an urgent health problem to be solved worldwide. Unfortunately, the exact pathogenesis and pathophysiology of sepsis-induced cardiovascular dysfunction are not clear. As a research hotspot in recent years, competing endogenous RNA (ceRNA) networks are involved in the modulation of the pathophysiological progression of many diseases, including sepsis-related CVDs. Both long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) can specifically bind to microRNAs (miRNAs) as ceRNAs to target messenger RNAs (mRNAs), forming a ceRNA network composed of lncRNA/circRNA-miRNA-mRNA. This review demonstrates the potential regulatory mechanism of the ceRNA networks in sepsis-induced cardiovascular toxicity, hoping to provide novel therapeutic strategies and monitoring targets for sepsis-related CVDs.

Keywords

cardiovascular

sepsis

competing endogenous RNA

long noncoding RNA

circular RNA

microRNA

Funding

2022NSFSC1404/Natural Science Foundation of Sichuan

2023NSFSC0694/Natural Science Foundation of Sichuan

S21026/Medical Scientific Project of Sichuan

Q21056/Medical Youth Innovation and Scientific Project of Sichuan

ZYKJJSC20-YYJC-2022-09/Ziyang Scientific Project

ZYKJJSC20-YYJC-2022-10/Ziyang Scientific Project

ZY2021S0030/Ziyang Social Science Project

ZY2021S0031/Ziyang Social Science Project

ZY2022S0055/Ziyang Social Science Project

ZY2022S0056/Ziyang Social Science Project

Figures

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Fig. 1.

Pathophysiological mechanism of septic cardiovascular diseases. Septic toxicity often causes systolic and diastolic dysfunction of the heart and vessels. The main mechanisms of septic cardiomyopathy include excessive inflammation, oxidative response, metabolic energy impairment, endoplasmic reticulum stress, and abnormal cell death. In addition, sepsis induced vascular dysfunction is associated with glycocalyx damage, endothelial injury, and vascular dystonia, leading to vascular paralysis and microcirculation disturbances. ATF6, activating transcription factor 6; ATP, adenosine 5’-triphosphate; CF, cell factor; CTLD, C-type lectin-like domain; DAMPs, danger-associated molecular patterns; ICAM1, intercellular cell adhesion molecule-1; IL, interleukin; IRE1 $\alpha{}$ , inositol-requiring kinase 1 $\alpha{}$ ; NF- $\kappa{}$ B, nuclear factor- $\kappa{}$ B; NLRs, NOD-like receptors; PAMPs, pathogen-associated molecular patterns; PERK, protein kinase R-like endoplasmic reticulum kinase; PRRs, pattern recognition receptors; ROS, reactive oxygen species; TGF- $\beta{}$ , transforming growth factor- $\beta{}$ ; TLR, toll-like receptor; TNF- $\alpha{}$ , tumor necrosis factor- $\alpha{}$ .

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Rev. Cardiovasc. Med. Print ISSN 1530-6550 Electronic ISSN 2153-8174