Post-stroke depression (PSD) is a complex mood disorder that emerges in individuals following a stroke, characterized by the development of depressive symptoms. The pathogensis of PSD is diverse, with inflammation playing a vital role in its onset and progression. Emerging evidence suggests that microglial activation, astrocyte responses, nuclear factor κB(NF-κB) signaling, dysregulation of the hypothalamic pituitary adrenal (HPA) axis, alterations in brain-derived neurotrophic factor (BDNF) expression, neurotransmitter imbalances, adenosine triphosphate (ATP) and its receptors and oxidative stress are intricately linked to the pathogenesis of PSD. The involvement of inflammatory cytokines in these processes highlights the significance of the inflammatory pathway. Integrating these hypotheses, the inflammatory mechanism offers a novel perspective to expand therapeutic strategies for PSD.