MicroRNAs regulate microglial polarization and influence the neuroinflammatory response induced by intracerebral hemorrhage

Intracerebral hemorrhage is a common central nervous system disease characterized by a high incidence, fatality and disablement rate. Currently, there is no specific treatment available for this disease, making it a major clinical challenge to overcome. Following an intracerebral hemorrhage event, there is a leakage of blood components from blood vessels into the brain. This leads to the activation of microglia, which are specialized cells of the innate immune system. Consequently, these cells release a plethora of inflammatory mediators. Neuroinflammation in the adjacent vicinity of the hematoma and throughout the entire brain can arise due to the interference caused by microglia and inflammatory mediators. The extent of such inflammation is intricately linked to secondary brain injury as well as the recovery of brain function. Over the past few years, several investigations have showcased the crucial function of microRNAs in governing disorders of the central nervous system. This is specifically relevant when considering the pathophysiological progression of intracerebral hemorrhage and its associated neuroinflammatory cascade. By manipulating the expression of microRNAs, these agents have the ability to impact the behavior of immune cells and regulate the post-intracerebral hemorrhage neuroinflammatory reaction. Consequently, this control could potentially aid in mitigating the neurological functional deterioration arising from secondary brain injury brought about by intracerebral hemorrhage. Henceforth, the exploration of microRNAs as plausible molecular targets to address intracerebral hemorrhage shall furnish novel concepts and unveil untrodden avenues for its forthcoming treatment.