The innate immune system, as the host’s first line of defense against intruders, plays a critical role in recognizing, identifying, and reacting to a wide range of microbial intruders. There is increasing evidence that mitochondrial stress is a major initiator of innate immune responses. When mitochondria’s integrity is disrupted or dysfunction occurs, the mitochondria’s contents are released into the cytosol. These contents, like reactive oxygen species, mitochondrial DNA, and double-stranded RNA, among others, act as damage-related molecular patterns (DAMPs) that can bind to multiple innate immune sensors, particularly pattern recognition receptors, thereby leading to inflammation. To avoid the production of DAMPs, in addition to safeguarding organelles integrity and functionality, mitochondria may activate mitophagy or apoptosis. Moreover, mitochondrial components and specific metabolic regulations modify properties of innate immune cells. These include macrophages, dendritic cells, innate lymphoid cells, and so on, in steady state or in stimulation that are involved in processes ranging from the tricarboxylic acid cycle to oxidative phosphorylation and fatty acid metabolism. Here we provide a brief summary of mitochondrial DAMPs’ initiated and potentiated inflammatory response in the innate immune system. We also provide insights into how the state of activation, differentiation, and functional polarization of innate immune cells can be influenced by alteration to the metabolic pathways in mitochondria.

Neurodegenerative diseases are a class of incurable and debilitating diseases characterized by progressive degeneration and death of cells in the central nervous system. They have multiple underlying mechanisms; however, they all share common degenerative features, such as mitochondrial dysfunction. According to recent studies, neurodegenerative diseases are associated with the accumulation of dysfunctional mitochondria. Selective autophagy of mitochondria, called mitophagy, can specifically degrade excess or dysfunctional mitochondria within cells. In this review, we highlight recent findings on the role of mitophagy in neurodegenerative disorders. Multiple studies were collected, including those related to the importance of mitochondria, the mechanism of mitophagy in protecting mitochondrial health, and canonical and non-canonical pathways in mitophagy. This review elucidated the important function of mitophagy in neurodegenerative diseases, discussed the research progress of mitophagy in neurodegenerative diseases, and summarized the role of mitophagy-related proteins in neurological diseases. In addition, we also highlight pharmacological advances in neurodegeneration.

BACKGROUND: Patent foramen ovale (PFO) and obstructive sleep apnea (OSA) are independent risk factors for young conscious stroke which may also be concomitant symptoms with it. But there is no sufficient attention on these phenomena. OBJECTIVE: To investigate the relationship between PFO, OSA and young stroke, and to look for proper treatment. METHODS: Three patients with young conscious stroke were reported, each of them was combined with PFO and OSA. All patients were diagnosed as wake-up stroke (WUS). Contrast-enhanced transcranial doppler ultrasound (c-TCD) and polysomnography (PSG) test were used for auxiliary diagnosis. RESULTS: Right-to-left shunts and moderate to severe sleep apnea were observed. Increased body mass index (BMI), hemoglobin (HGB) and hematocrit (HCT) index were also observed. After continuous positive airway pressure (CPAP) therapy, the number of microbubbles was reduced in one patient. CONCLUSIONS: These suggest that coexistence of PFO and OSA may associate with a greater risk of youth stroke. Decrease risk of stroke might occur if treating with CPAP in patients with OSA.