Key result
Pollutants and industrial toxins show potential links to molecular and epigenetic mechanisms of cardiomyopathy.
Why the study?
Industrial pollutants and toxins are recognized contributors to cardiovascular disease onset and progression, highlighting the need to understand molecular-genetic and epigenetic mechanisms in cardiomyopathies to guide potential pharmacological strategies.
This review outlines potential molecular and epigenetic mechanisms linking industrial pollutants to the development and progression of cardiomyopathies.
Hypothesis-generating for pollutant roles in cardiomyopathies; does not support practice changes pending prospective evidence.
The article presents a review of current scientific articles related to a few particular questions of molecular-genetic and epigenetic pathogenesis of some cardiomyopathy types that can be the object of interest assuming potential associations with pathophysiological mechanisms of pollutants and industrial toxins impaction. The possible benefits may arise from that kind of approach due to the fact that toxic agents in question are generally recognized at the moment as one of the cardiovascular disease onset and progression factors. The need for multidirectional theoretical developments targeting potential pharmacology methods aimed to at least partially eliminate such a challenge becomes more and more apparent. We focused on mTOR function chains, translation factor eIF4E and splicing regulator RBM20 interconnected with RAAS and T3 regulatory cascades. A part of our attention was also concentrated on cardiomyocytes methylome profiling in connection with pollutant toxicodynamics and cardiomyopathies pathogenesis.
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Nechaev et al. (2023) conducted a review in Cardiomyopathies. A review of molecular-genetic and epigenetic pathogenesis of cardiomyopathies highlights potential associations with pathophysiological mechanisms of pollutants and industrial toxins.
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