Ischemic stroke, a leading cause of disability and mortality worldwide, is a complex cerebrovascular event with outcomes heavily influenced by the inflammatory response. This response, triggered by cerebral ischemia, plays a critically dual role: while exacerbating secondary damage in the acute phase, it is also essential for tissue repair and recovery. The identification and study of inflammation-related biomarkers have thus emerged as a pivotal area of research, offering new avenues for early diagnosis, prognostic assessment, and targeted therapy in the pursuit of precision medicine for stroke.
The Dual-Nature Inflammatory Response Post-Stroke
The inflammatory cascade begins with the release of damage-associated molecular patterns (DAMPs) from dying neurons in the infarct core. These DAMPs activate innate immune pathways, such as Toll-like receptors (TLRs) and the NF-κB signaling pathway, leading to a surge in pro-inflammatory cytokines like IL-1β, TNF-α, and IL-6. This response promotes the infiltration of peripheral immune cells, disrupts the blood-brain barrier (BBB), and amplifies oxidative stress, causing further neuronal death. Conversely, a moderated inflammatory response, driven by anti-inflammatory cytokines like IL-10 and TGF-β, is crucial for facilitating nerve regeneration and angiogenesis, highlighting the need for balanced therapeutic intervention.
Key Inflammatory Biomarkers and Their Mechanisms
The review systematically categorizes and explains the roles of various biomarkers:
