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

Area of Science:

• Cardiovascular Research
• Immunology
• Fibrosis Mechanisms

Background:

• Cardiovascular diseases (CVDs) are increasingly viewed as chronic conditions driven by inflammation and fibrosis.
• Understanding the transition from acute inflammation to pathological fibrosis is crucial for developing effective treatments.

Purpose of the Study:

• To elucidate emerging mechanisms governing the inflammation-to-fibrosis transition in CVDs.
• To highlight novel therapeutic strategies targeting the inflammation-fibrosis axis.

Main Methods:

• Review of cellular crosstalk (neutrophils, macrophages, fibroblasts, myofibroblasts).
• Analysis of extracellular matrix (ECM) remodeling and dysregulated immune responses.
• Exploration of cell plasticity (macrophage polarization, fibroblast-to-myofibroblast transition).
• Investigation of key signaling pathways (TGF-β) and factors (hypoxia, noncoding RNAs).

Main Results:

• Dysregulated immune responses and ECM remodeling create a pathogenic feedback loop, leading to myocardial stiffening and adverse cardiac remodeling.
• Cellular plasticity and specific molecular pathways (TGF-β, hypoxia, noncoding RNAs) are key drivers of fibrosis progression.

Conclusions:

• Next-generation therapies (immunometabolic, epigenetic reprogramming, gene editing, cell-based, nanomedicine) show promise in interrupting the inflammation-fibrosis axis.
• Targeting these pathways offers potential to reverse maladaptive remodeling, restore cardiac function, and transform CVD treatment.