CeRNA plays a key role in the induction of cardiovascular diseases by environmental endocrine disruptor exposure

TL;DR

This study explores how ceRNAs contribute to cardiovascular diseases caused by environmental endocrine disruptors, revealing potential new targets for treatment.

Contribution

The study systematically identifies ceRNA pathways involved in EDC-induced cardiovascular diseases, offering new insights into disease mechanisms.

Findings

CeRNA-mediated effects of EDCs on CVDs occur through four distinct signaling pathways.

EDC exposure alters mRNAs and proteins in ceRNA networks, leading to cardiomyopathy.

CeRNAs upregulate nitric oxide or reactive oxygen species, contributing to vascular diseases.

Abstract

Competing endogenous RNAs (ceRNAs) represent a novel mechanism involving interactions among different RNAs, playing a crucial role in the gene regulatory networks throughout the life cycle. CeRNAs are implicated in cardiovascular diseases (CVDs) caused by environmental endocrine disruptors (EDCs); however, existing studies are not yet systematic, and the mechanisms underlying their effects remain unclear.

This study aimed to systematically elucidate the role of ceRNAs in EDC-induced CVDs and provide valuable insights regarding disease mechanisms and developing new therapeutic strategies.

Comprehensive searches for research related to EDC-induced cardiovascular diseases were conducted across PubMed, Web of Science, and ScienceDirect databases. Eligible studies were screened, and those containing information on the regulatory mechanisms of ceRNAs were extracted and analyzed.

Notably, ceRNA-mediated effects of EDC exposure on CVDs mainly occurred through four pathways. First, upon exposure to EDCs, micro RNAs, messenger RNAs (mRNAs), long-chain non-coding RNAs, circular RNAs are differentially regulated, activating signaling pathways such as nuclear factor erythroid 2-related factor 2 and p38 mitogen-activated protein kinase/nuclear factor-κB, which lead to atherosclerosis. Second, EDC exposure alters mRNAs and proteins involved in ceRNA networks, activating the PTEN-induced kinase 1/Parkin and transforming growth factor-β1/LIM domain kinase 1 signaling pathways, leading to cardiomyopathy. Third, EDCs increase ceRNA-related mRNA levels, thereby raising the risk of CVDs. Lastly, ceRNAs participate in EDC exposure to upregulate nitric oxide or reactive oxygen species, ultimately causing vascular diseases.

Altogether, the findings of this study show that ceRNAs hold significant potential for identifying target genes and signaling pathways associated with CVDs, which may facilitate deeper studies into CVD management.

The online version contains supplementary material available at https://doi.org/10.1265/ehpm.25-00165.

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