Stroke is a devastating disease with high mortality and disability rates. Previous research has established that mitochondria, as major regulators, are both influenced by stroke, and further regulated the development of poststroke injury. Mitochondria are involved in several biological processes such as energy generation, calcium homeostasis, immune response, apoptosis regulation, and reactive oxygen species (ROS) generation. Meanwhile, mitochondria can evolve into various quality control systems, including mitochondrial dynamics (fission and fusion) and mitophagy, to maintain the homeostasis of the mitochondrial network. Various activities of mitochondrial fission and fusion are associated with mitochondrial integrity and neurological injury after stroke. Additionally, proper mitophagy seems to be neuroprotective for its effect on eliminating the damaged mitochondria, while excessive mitophagy disturbs energy generation and mitochondria-associated signal pathways. The balance between mitochondrial dynamics and mitophagy is more crucial than the absolute level of each process. A neurovascular unit (NVU) is a multidimensional system by which cells release multiple mediators and regulate diverse signaling pathways across the whole neurovascular network in a way with a high dynamic interaction. The turbulence of mitochondrial quality control (MQC) could lead to NVU dysfunctions, including neuron death, neuroglial activation, blood–brain barrier (BBB) disruption, and neuroinflammation. However, the exact changes and effects of MQC on the NVU after stroke have yet to be fully illustrated. In this review, we will discuss the updated mechanisms of MQC and the pathophysiology of mitochondrial dynamics and mitophagy after stroke. We highlight the regulation of MQC as a potential therapeutic target for both ischemic and hemorrhagic stroke.

Sepsis is a leading cause of intensive care unit admission and death worldwide. Most surviving patients show acute or chronic mental disorders, which are known as sepsis-associated encephalopathy (SAE). Although accumulating studies in the past two decades focused on the pathogenesis of SAE, a systematic review of retrospective studies which exclusively focuses on the inflammatory mechanisms of SAE has been lacking yet. This review summarizes the recent advance in the field of neuroinflammation and sheds light on the activation of microglia in SAE. Activation of microglia predominates neuroinflammation. As the gene expression profile changes, microglia show heterogeneous characterizations throughout all stages of SAE. Here, we summarize the systemic inflammation following sepsis and also the relationship of microglial diversity and neuroinflammation. Moreover, a collection of neuroinflammation-related dysfunction has also been reviewed to illustrate the possible mechanisms for SAE. In addition, promising pharmacological or non-pharmacological therapeutic strategies, especially those which target neuroinflammation or microglia, are also concluded in the final part of this review. Collectively, clarification of the vital relationship between neuroinflammation and SAE-related mental disorders would significantly improve our understanding of the pathophysiological mechanisms in SAE and therefore provide potential targets for therapies of SAE aimed at inhibiting neuroinflammation.

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