Molecular biomarkers for intracerebral hemorrhage: bridging pathophysiology and precision medicines

Intracerebral hemorrhage (ICH) is a highly destructive subtype of stroke, characterized by high mortality and disability rates, and remains a major clinical challenge due to limited effective treatments, hyperacute diagnostic tools, and insufficient prognostic strategies. Current approaches, primarily based on clinical symptoms and neuroimaging, effectively identify location but lack sensitivity for early risk assessment and dynamic disease monitoring. Molecular biomarkers have shown great promise in elucidating ICH pathogenesis, enhancing diagnostic sensitivity, enabling dynamic disease tracking, and improving outcome prediction. However, clinical translation remains hindered by challenges in standardization, specificity, and validation frameworks. This review systematically summarizes recent advances in biomarker research related to ICH, with a particular focus on key etiological mechanisms such as hypertension and cerebral amyloid angiopathy, as well as critical pathophysiological processes including hematoma expansion, perihematomal edema, neuroinflammation, and oxidative stress. We further explore the emerging role of multi-omics technologies, including genomics, transcriptomics, proteomics, and metabolomics, in identifying ICH specific molecular signatures. Emphasis is placed on the potential clinical utility of these biomarkers in high-risk population screening, early diagnosis, disease monitoring, and outcome prediction. Moreover, we propose the development of a disease-specific, multidimensional biomarker panel that integrates advanced neuroimaging and artificial intelligence-based analytical strategies. This approach aims to accelerate the clinical translation of biomarkers into precision medicine, supporting personalized therapeutic decision-making, preventing the onset of ICH, and improving outcomes. It further promotes a paradigm shift in ICH management from passive treatment to proactive prevention and control.