Abstract：
Intracranial hemorrhage (ICH) causes numerous neurological deficits and deaths worldwide each year, leaving a significant health burden on the public. The pathophysiology of ICH is complicated, and involves both primary and secondary injury. Hematoma, as the prime pathology of ICH, undergoes metabolism and triggers biochemical and biomechanical alterations in the brain, leading to secondary injury. Past endeavors mainly aimed at biochemical-initiated mechanisms for causing secondary injury have made limited progress in recent years, although ICH itself is also highly biomechanics-related. The discovery of the mechanical-activated cation channel Piezo1 provides a new avenue to further explore underlying mechanisms of secondary injury. The current article reviews the structure and gating mechanisms of Piezo1, its roles in the physiology/pathophysiology of neurons, astrocytes, microglia, and bone-marrow-derived macrophages, and especially its roles in erythrocytic turnover and iron metabolism, revealing a potential interplay between the biomechanics and biochemistry of hematoma in ICH. Collectively, these advances provide deeper insights into the secondary injury of ICH and lay the foundations for future research.
摘要：
颅内出血（ICH）每年在全球范围内导致许多神经功能缺损和死亡。给公众留下了巨大的健康负担。ICH的病理生理学很复杂,涉及原发性和继发性损伤。血肿,作为ICH的主要病理学，经历新陈代谢并触发大脑中的生化和生物力学改变，导致二次伤害。过去主要针对引起继发性损伤的生化启动机制的努力近年来取得了有限的进展，虽然ICH本身也与生物力学高度相关。机械激活阳离子通道Piezo1的发现为进一步探索继发性损伤的潜在机制提供了新的途径。本文综述了Piezo1的结构和门控机制，其在神经元生理/病理生理学中的作用，星形胶质细胞,小胶质细胞,和骨髓来源的巨噬细胞，尤其是它在红细胞更新和铁代谢中的作用，揭示ICH血肿的生物力学和生物化学之间的潜在相互作用。总的来说，这些进展为ICH继发性损伤提供了更深入的见解,并为未来的研究奠定了基础.
