Connection between oxidative stress and subcellular organelle in subarachnoid hemorrhage: Novel mechanisms and therapeutic implications

Spontaneous subarachnoid hemorrhage (SAH) is one of the most devastating forms of stroke, with limited treatment modalities and poor patient outcomes. Previous studies have proposed multiple prognostic factors; however, relative research on treatment has not yet yielded favorable clinical outcomes. Moreover, recent studies have suggested that early brain injury (EBI) occurring within 72 h after SAH may contribute to its poor clinical outcomes. Oxidative stress is recognized as one of the main mechanisms of EBI, which causes damage to various subcellular organelles, including the mitochondria, nucleus, endoplasmic reticulum (ER), and lysosomes. This could lead to significant impairment of numerous cellular functions, such as energy supply, protein synthesis, and autophagy, which may directly contribute to the development of EBI and poor long-term prognostic outcomes. In this review, the mechanisms underlying the connection between oxidative stress and subcellular organelles after SAH are discussed, and promising therapeutic options based on these mechanisms are summarized.

Automated summary

Spontaneous subarachnoid hemorrhage (SAH) is a devastating form of stroke with limited treatment options and poor patient outcomes. Early brain injury (EBI) occurring within 72 hours after SAH has been suggested to contribute to its poor clinical outcomes. Oxidative stress, which damages subcellular organelles, such as mitochondria and endoplasmic reticulum (ER), is recognized as a main mechanism of EBI. This review discusses the connection between oxidative stress and subcellular organelles after SAH and summarizes promising therapeutic options based on these mechanisms.