Why the study?
Crosstalk between cardiac and renal systems in cardiorenal syndromes is not completely understood, and multi-omics approaches may reveal new mechanisms implicated in this pathogenesis.
Multi-omics approaches offer new insights into the complex molecular mechanisms underlying cardiorenal crosstalk beyond traditional hemodynamic parameters.
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CRS mechanisms remain incompletely understood; leaves open targeted research on inflammatory and endothelial pathways.
Cardiorenal syndromes (CRS) include a scenario of clinical interactions characterized by the heart and kidney dysfunction. The crosstalk between cardiac and renal systems is clearly evidenced but not completely understood. Multi-factorial mechanisms leading to CRS do not involve only hemodynamic parameters. In fact, in recent works on organ crosstalk endothelial injury, the alteration of normal immunologic balance, cell death, inflammatory cascades, cell adhesion molecules, cytokine and chemokine overexpression, neutrophil migration, leukocyte trafficking, caspase-mediated induction of apoptotic mechanisms and oxidative stress has been demonstrated to induce distant organ dysfunction. Furthermore, new alternative mechanisms using the multi-omics approach may be implicated in the pathogenesis of cardiorenal crosstalk. The study of "omics" modifications in the setting of cardiovascular and renal disease represents an emerging area of research. Over the last years, indeed, many studies have elucidated the exact mechanisms involved in gene expression and regulation, cellular communication and organ crosstalk. In this review, we analyze epigenetics, gene expression, small non-coding RNAs, extracellular vesicles, proteomics, and metabolomics in the setting of CRS.
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Virzì et al. (2019) studied this question.
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