Targeting Inflammation and Fibrosis in Cardiovascular Disease: Emerging Mechanisms and Therapies

Cardiovascular diseases are influenced by complex interactions between inflammation and fibrosis.

• Acute inflammation can transition to pathological fibrosis through cellular interactions among neutrophils, macrophages, fibroblasts, and myofibroblasts.
• Dysregulated immune responses and changes in the extracellular matrix may create a feedback loop that leads to myocardial stiffening.
• The plasticity of immune and stromal cells, such as macrophage polarization and the conversion of fibroblasts to myofibroblasts, is crucial in this process.
• Factors like TGF-β signaling, hypoxia, and noncoding RNAs are implicated in the development of fibrosis in cardiovascular diseases.
• Next-generation therapies aim to disrupt the inflammation-fibrosis cycle through various approaches, including immunometabolic and epigenetic reprogramming.

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