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Scarred by Fibrosis: The Heart-Kidney Disease Connection
Juliana H Boukhaled1,2, Emily M Martin3,4, Nathalie Gayrard1
1RD Néphrologie, Montpellier, France;
Insights
Cardiorenal syndrome (CRS) involves heart and kidney dysfunction. Fibrosis, driven by fibroblast activity, is a key factor in CRS progression, impacting both organs and offering therapeutic targets.
Area of Science:
- Cardiology
- Nephrology
- Fibrosis Research
Background:
- Cardiorenal syndrome (CRS) is a complex condition involving heart and kidney dysfunction.
- Hemodynamic changes are known contributors, but structural alterations also play a significant role.
- Fibrosis, characterized by inflammation and excessive extracellular matrix production, is a common pathological feature in CRS affecting both organs.
Purpose of the Study:
- To review the crucial role of fibroblast activities in the onset and progression of cardiorenal fibrosis.
- To explore how fibrosis in one organ exacerbates dysfunction in the other.
- To identify key signaling pathways, biomarkers, and therapeutic strategies targeting fibroblast activity in CRS.
Main Methods:
- Literature review focusing on fibroblast-mediated fibrosis in cardiorenal syndrome.
- Analysis of pathological signaling pathways involved in cardiorenal fibrosis.
- Evaluation of extracellular matrix-derived biomarkers for clinical management and drug development.
Main Results:
- Fibroblast activation and excessive extracellular matrix deposition are central to cardiorenal fibrosis.
- Fibrosis in the heart or kidneys can initiate or worsen dysfunction in the contralateral organ.
- Specific signaling pathways and ECM-derived biomarkers are implicated in CRS pathogenesis.
Conclusions:
- Fibroblast activity is a critical determinant of cardiorenal fibrosis and CRS progression.
- Targeting fibroblast pathways presents promising therapeutic opportunities for managing CRS.
- Further research into ECM biomarkers can aid in clinical management and drug discovery for CRS.
Abstract:
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.
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