Key result
Inflammation alongside neurohormonal, endocrine, and immune dysregulation drives cardiorenal syndrome pathogenesis.
Why the study?
In cardiorenal syndrome, multiple pathophysiological processes beyond hemodynamic parameters are implicated, motivating an overview of neurohormonal, endocrine, and immune dysregulation and inflammation.
This review summarizes the complex pathophysiological mechanisms, including neurohormonal and immune dysregulation, underlying cardiorenal syndrome.
May guide mechanistic research in cardiorenal syndrome; leaves open translation to targeted therapies.
"Organ crosstalk" is the complex physiological communication between different body systems, and it is necessary for the optimal equilibrium and functioning of the organism. In particular, heart and kidney function is tightly connected, and interplay between these two organs occurs through a vast array of dynamic and bidirectional mechanisms. The term cardiorenal syndrome (CRS) indicates an interaction between the heart and kidneys in acute and chronic disease settings. In all types of CRS, multiple pathophysiological processes are implicated in the initiation and progression of organ injury. In addition to hemodynamic parameters, endothelial injury, immunological imbalance, cell death, inflammatory cascades, oxidative stress, neutrophil migration, leukocyte trafficking, caspase-mediated apoptosis, extracellular vesicles, small noncoding RNAs, and epigenetics play pivotal roles in the development of CRS. In this review, we will focus on neurohormonal, endocrine, and immune dysregulation and inflammation as mechanisms involved in the pathogenesis of CRS.
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Clementi et al. (2019) conducted a review in Cardiorenal syndrome. Neurohormonal, endocrine, and immune dysregulation, along with inflammation, play pivotal roles in the pathogenesis of cardiorenal syndrome.
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