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Heart failure (HF) is a condition characterized by high morbidity, mortality, and a substantial healthcare burden, in which inflammation plays a pivotal role. This review provides a comprehensive overview of inflammation in HF progression, highlighting the dynamic alterations in immune cell populations-such as monocytes/macrophages and neutrophils-and regulatory mechanisms of key signaling pathways, including JAK and NLRP3. Furthermore, the clinical relevance of inflammatory biomarkers in predicting disease prognosis is also discussed. Emerging evidence indicates that exercise intervention can enhance cardiac function by promoting the expression of anti-inflammatory cytokines (e.g., IL-10) and mitigating myocardial fibrosis, oxidative stress, and apoptosis. Future studies should investigate how exercise modulates critical inflammatory pathways-such as TLR/MyD88/NF-κB and the NLRP3 inflammasome-and aim to establish personalized exercise protocols tailored to patients' inflammatory profiles and disease stages. Such insights may pave the way for innovative therapeutic strategies in HF management.
Luo et al. (Mon,) studied this question.