Key result
This review hypothesizes and summarizes the interplay between TGF-β, KLF5, and the glycolysis pathway in the pathogenesis of cardiac fibrosis to identify future therapeutic targets.
Why the study?
The interplay among TGF-β, KLF5, and the metabolic process in glycolysis during cardiac fibrosis pathogenesis remains indistinct, limiting options to reduce or reverse fibrosis.
This review proposes a novel hypothetical framework linking TGF-β, KLF5 signaling, and glycolysis in the development of cardiac fibrosis, highlighting potential new targets for heart failure therapy.
Hypothesis-generating for cardiac fibrosis therapies; leaves open clinical translation pending prospective validation.
The accumulation of fibrosis in cardiac tissues is one of the leading causes of heart failure. The principal cellular effectors in cardiac fibrosis are activated fibroblasts and myofibroblasts, which serve as the primary source of matrix proteins. TGF-β signaling pathways play a prominent role in cardiac fibrosis. The control of TGF-β by KLF5 in cardiac fibrosis has been demonstrated for modulating cardiovascular remodeling. Since the expression of KLF5 is reduced, the accumulation of fibrosis diminishes. Because the molecular mechanism of fibrosis is still being explored, there are currently few options for effectively reducing or reversing it. Studying metabolic alterations is considered an essential process that supports the explanation of fibrosis in a variety of organs and especially the glycolysis alteration in the heart. However, the interplay among the main factors involved in fibrosis pathogenesis, namely TGF-β, KLF5, and the metabolic process in glycolysis, is still indistinct. In this review, we explain what we know about cardiac fibroblasts and how they could help with heart repair. Moreover, we hypothesize and summarize the knowledge trend on the molecular mechanism of TGF-β, KLF5, the role of the glycolysis pathway in fibrosis, and present the future therapy of cardiac fibrosis. These studies may target therapies that could become important strategies for fibrosis reduction in the future.
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Methatham et al. (2022) conducted a review in Cardiac fibrosis. TGF-β, KLF5, and glycolysis pathway was evaluated. This review hypothesizes and summarizes the interplay between TGF-β, KLF5, and the glycolysis pathway in the pathogenesis of cardiac fibrosis to identify future therapeutic targets.
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