Key result
Targeting fibroblast signaling pathways alongside localized drug delivery shows potential to reduce cardiac fibrosis.
Why the study?
Cardiac fibrosis contributes to contractile dysfunction and heart failure progression, necessitating an understanding of the cellular effectors, molecular pathways, and strategies to monitor fibroblast-targeting drugs.
This review highlights the cellular effectors and molecular pathways in cardiac fibrosis and suggests strategies for monitoring drugs targeting cardiac fibroblasts.
Should not yet change fibrosis management; leaves open clinical validation of pathway-targeted delivery strategies.
Cardiac fibrosis is characterized by extracellular matrix deposition in the cardiac interstitium, and this contributes to cardiac contractile dysfunction and progression of heart failure. The main players involved in this process are the cardiac fibroblasts, which, in the presence of pro-inflammatory/pro-fibrotic stimuli, undergo a complete transformation acquiring a more proliferative, a pro-inflammatory and a secretory phenotype. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis and suggests potential strategies to monitor the effects of specific drugs designed to slow down the progression of this disease by specifically targeting the fibroblasts.
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Garoffolo et al. (2021) conducted a review in Cardiac fibrosis and heart failure. Targeting specific intracellular signaling pathways in cardiac fibroblasts, combined with advanced imaging and localized drug delivery, offers potential strategies to reduce cardiac fibrosis.
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