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Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the abilit...

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Autores principales: Wallace, David R., Taalab, Yasmeen M., Heinze, Sarah, Tariba Lovaković, Blanka, Pizent, Alica, Renieri, Elisavet, Tsatsakis, Aristidis, Farooqi, Ammad Ahmad, Javorac, Dragana, Andjelkovic, Milena, Bulat, Zorica, Antonijević, Biljana, Buha Djordjevic, Aleksandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226740/
https://www.ncbi.nlm.nih.gov/pubmed/32272672
http://dx.doi.org/10.3390/cells9040901
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author Wallace, David R.
Taalab, Yasmeen M.
Heinze, Sarah
Tariba Lovaković, Blanka
Pizent, Alica
Renieri, Elisavet
Tsatsakis, Aristidis
Farooqi, Ammad Ahmad
Javorac, Dragana
Andjelkovic, Milena
Bulat, Zorica
Antonijević, Biljana
Buha Djordjevic, Aleksandra
author_facet Wallace, David R.
Taalab, Yasmeen M.
Heinze, Sarah
Tariba Lovaković, Blanka
Pizent, Alica
Renieri, Elisavet
Tsatsakis, Aristidis
Farooqi, Ammad Ahmad
Javorac, Dragana
Andjelkovic, Milena
Bulat, Zorica
Antonijević, Biljana
Buha Djordjevic, Aleksandra
author_sort Wallace, David R.
collection PubMed
description Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)—short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain—a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).
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spelling pubmed-72267402020-05-18 Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development Wallace, David R. Taalab, Yasmeen M. Heinze, Sarah Tariba Lovaković, Blanka Pizent, Alica Renieri, Elisavet Tsatsakis, Aristidis Farooqi, Ammad Ahmad Javorac, Dragana Andjelkovic, Milena Bulat, Zorica Antonijević, Biljana Buha Djordjevic, Aleksandra Cells Review Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)—short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain—a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs). MDPI 2020-04-07 /pmc/articles/PMC7226740/ /pubmed/32272672 http://dx.doi.org/10.3390/cells9040901 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Wallace, David R.
Taalab, Yasmeen M.
Heinze, Sarah
Tariba Lovaković, Blanka
Pizent, Alica
Renieri, Elisavet
Tsatsakis, Aristidis
Farooqi, Ammad Ahmad
Javorac, Dragana
Andjelkovic, Milena
Bulat, Zorica
Antonijević, Biljana
Buha Djordjevic, Aleksandra
Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
title Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
title_full Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
title_fullStr Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
title_full_unstemmed Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
title_short Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
title_sort toxic-metal-induced alteration in mirna expression profile as a proposed mechanism for disease development
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226740/
https://www.ncbi.nlm.nih.gov/pubmed/32272672
http://dx.doi.org/10.3390/cells9040901
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