This review highlights the central role of fibrosis and fibroblast activation in the pathophysiology of cardiorenal syndrome, identifying potential biomarkers and therapeutic targets.
Cardiorenal syndrome (CRS) represents a complex interplay of pathophysiological processes that create a self-perpetuating cycle of heart and kidney dysfunction. While it is clearly understood how hemodynamic changes connect pathogenesis in the two organs, other processes are also in play. Some are the structural changes involving both the cellular and extracellular compartments that precede functional alterations. Fibrosis, which is initiated by an inflammatory response triggering myofibroblast activation and excessive extracellular matrix production, is a common denominator of heart and kidney pathology in CRS. This review focuses on fibroblast activities as a crucial factor in disease onset and progression in CRS. We explore how fibrosis in one organ can trigger or worsen dysfunction in the other organ, and we describe the key pathological signaling pathways of cardiorenal fibrosis, the extracellular matrix-derived biomarkers that can aid clinical management and drug development, and the therapeutic opportunities that can be beneficial in CRS by targeting fibroblast activities.
Boukhaled et al. (Tue,) studied this question.