Key result
Curcumin and analogs show potential to reverse myocardial fibrosis by regulating extracellular matrix metabolism.
Why the study?
Research on the anti-myocardial fibrotic effects of curcumin and its analogs is currently fragmented despite their broad therapeutic potential.
Do curcumin and its analogs improve myocardial fibrosis?
Do curcumin and its analogs improve myocardial fibrosis?
Curcumin and its analogs show promising therapeutic potential for reversing myocardial fibrosis, providing a theoretical basis for future development and application.
Hypothesis-generating for curcumin analogs in myocardial fibrosis; prospective trials needed before clinical consideration.
Myocardial fibrosis is a pathological process characterized by the abnormal accumulation of extracellular matrix, forming pathological scars, due to excessive activation of cardiac fibroblasts during injury repair. This process leads to cardiac stiffening, disruption of electrical conduction, and ultimately, cardiac dysfunction. Curcumin effectively reverses myocardial fibrosis by regulating the metabolic network of extracellular matrix synthesis and degradation. Its analogs, through chemical modification to curcumin, retain and even enhance therapeutic activity meanwhile overcoming inherent limitations of natural curcumin. Given the broad therapeutic potential of curcumin and its analogs against myocardial fibrosis, and the fragmented nature of current research in this field, this review retrieved research on the anti‐myocardial fibrotic effects of curcumin and its analogs published in the last decade from English databases, while a small number of references are older. To establish a theoretical basis for advancing the development and application of curcumin and its analogs, this review synthesizes essential information regarding their properties, mechanisms, pharmacological effects, and therapeutic potential.
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Wang et al. (2026) conducted a review in Myocardial fibrosis. Curcumin and its analogs was evaluated. Curcumin and its analogs demonstrate therapeutic potential in reversing myocardial fibrosis by regulating the metabolic network of extracellular matrix synthesis and degradation.
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