Coronary heart disease (CHD) affects millions of individuals worldwide and remains a leading cause of morbidity and mortality. It compromises quality of life primarily through myocardial ischemia resulting from progressive coronary arterial narrowing and contributes to a wide range of adverse clinical outcomes. Although current therapeutic strategies, including coronary revascularization, lipid-lowering therapy, and plaque stabilization, have substantially improved patient prognosis, they do not fully address the underlying immunopathological mechanisms driving disease progression. Increasing evidence suggests that immune-mediated inflammation and vascular injury play critical roles in the initiation, progression, and destabilization of atherosclerotic plaques, highlighting the immune system as a potential therapeutic target in CHD management. In this review, we summarize recent advances in our understanding of the contributions of innate and adaptive immune responses to CHD pathogenesis. Collectively, current evidence indicates that immune dysregulation is a central driver of atherogenesis and its clinical manifestations, supporting the development of targeted immunomodulatory strategies as promising approaches for the prevention and treatment of CHD.

Post-stroke cognitive impairment (PSCI) is a frequent and disabling consequence of stroke that limits long-term recovery and quality of life. Disruption of the hippocampal neurogenic niche may impair adult hippocampal neurogenesis (AHN), while exercise is increasingly recognized as a promising non-pharmacological strategy for cognitive rehabilitation. This review synthesizes evidence that exercise may shift the post-stroke hippocampal niche from a hostile to a permissive state through coordinated regulation of neuroinflammation, neurovascular integrity, and mitochondrial homeostasis. We distinguish increased progenitor proliferation from productive neurogenesis, defined by the survival, maturation, appropriate positioning, and functional integration of newborn neurons. Exercise may attenuate inflammatory signaling, support angiogenesis and blood–brain barrier repair, and improve mitochondrial biogenesis and quality control; however, much of the mechanistic evidence remains preclinical, and increases in early neurogenic markers do not by themselves establish functional neuronal integration or causality. Current clinical evidence supports cognitive benefits of exercise more strongly than it supports AHN as the indispensable mediator of those benefits. A productive-neurogenesis framework therefore provides a more rigorous basis for interpreting existing studies and designing future experiments that combine lineage tracing, temporally controlled neurogenesis ablation, circuit-level analysis, and domain-specific cognitive outcomes.