Key result
Oxidative stress, angiogenesis, and microRNAs regulate cardiac hypertrophy and offer potential targets for molecular therapies.
This review summarizes the molecular targets and signaling pathways involved in cardiac hypertrophy, highlighting potential avenues for nutritional and molecular therapies.
Supports targeted research on hypertrophy pathways; leaves open clinical translation pending prospective trials.
Cardiac hypertrophy is the major pathway by which neurohormonal and mechanical stimuli act upon cardiomyocytes which gives the response to these stimuli. It leads to heart failure and ventricular dilation which is the main root of mortality in the western world. Many molecular targets are controlling cardiac hypertrophy development which may influence the growth factors signaling, cytokine release and gene expression. Through clinical trials on different models, recent research shows that cardiac hypertrophy might be inhibited or reversed. These findings have developed a vast drive to recognize specific and novel regulators of cardiac hypertrophy. Many molecular targets and signaling modulators have been studied in this review that induce the hypertrophic response which may involve MAPK pathway, oxidative stress, calcineurin, Cardiac angiogenesis, serum protein concentration, microRNA, and periodontitis. For the treatment of cardiac hypertrophy, the scientific knowledge of these signaling pathways and factors may be translated into potential nutritional and molecular therapies for the betterment of this diseases. The current and previous knowledge of molecular markers can be compiled in this review for the treatment of the molecular pathogenesis of cardiac hypertrophy.
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Shad et al. (2021) conducted a review in Cardiac hypertrophy. Molecular targets and regulators was evaluated. Cardiac hypertrophy is regulated by multiple molecular pathways including oxidative stress, angiogenesis, and microRNAs, which represent potential targets for future molecular therapies.
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