Unravelling Cardiovascular Diseases: Pathogenesis and Therapies

Introduction: Cardiovascular diseases (CVDs) continue to be a leading cause of global mortality, with the contribution of inflammation and immune dysregulation recognized as central drivers in the pathogenesis. While traditional risk factors, such as hypertension, diabetes, obesity, and smoking, contribute significantly, recent evidence suggests that chronic inflammation and immune activation are key mechanisms contributing to atherosclerosis, heart failure, arrhythmias, and myocardial infarction. This review broadly assesses the inflammatory and immunological pathways, highlighting the cellular contributors, molecular mediators, and pathogenic cascades that are involved in the onset and progression of CVDs. The objective of the review is to explain the immune-inflammatory basis of CVDs and critically examine current and emerging therapeutic interventions targeting the aforementioned pathways. Using a strategic narrative review approach, recent clinical trials, preclinical studies, and relevant evidence have been analysed to present a detailed understanding of immune cell contribution, cytokine signaling, plaque formation, and endothelial dysfunction. Methodology: The present review was an organized examination of the existing literature related to the role of inflammation and immunomodulation and their respective therapeutic agents in cardiovascular diseases. This involved searching databases, including PubMed, Google Scholar, ScienceDirect, Elsevier, Bentham Science, and NIH and WHO resources, to identify pertinent articles. Results: Key findings indicate that proinflammatory cytokines like TNF-α, IL-6, and IL-1β, along with chemokines such as MCP-1, contribute to vascular injury, plaque formation, and myocardial remodeling. Immune cells, such as macrophages, dendritic cells, and lymphocytes, facilitate disease progression through cytokine release and maladaptive repair. Anti-inflammatory agents, including colchicine, statins, and targeted monoclonal antibodies (e.g., canakinumab), have shown promise in reducing cardiovascular events, though risks such as bleeding and infection remain. Discussion: The review assessed the interlinked inflammatory and immunological pathways in the pathogenesis of CVDs and identified the cellular and molecular mediators. It also examined current and emerging therapeutic interventions, covering recent clinical and preclinical trials and key findings that clarify immune cell roles, cytokine signalling, plaque formation, and endothelial dysfunction. Conclusion: This review highlights the need for proper immunotherapy in CVDs, supporting targeted modulation of chronic inflammation. Technology and science continue to explore future advancements in personalized medicine and immunomodulation to transform CVD management beyond traditional lipid- and pressure-centered strategies.