LncRNA SNHG11 induces ferroptosis in liver injury cells through miR-324-3p/GPX4 axis-mediated sepsis.

Sepsis is a kind of systemic inflammatory response syndrome caused by infection, which has high morbidity and mortality. Studies have shown that reducing sepsis-related liver injury and restoring liver function can reduce the morbidity and mortality of it. Current clinical treatment methods for sepsis have many disadvantages. Our study aimed to investigate the mechanism of sepsis-induced liver injury and to find a proper therapeutic target for sepsis. In this paper, we have found that when miR-324-3p was overexpressed, the inflammatory infiltration and and ferroptosis in liver injury cells aggravated. Further studies showed that overexpression of miR-324-3p could bind to the 3'-UTR of SNHG11 directly so as to decrease the expression level of SNHG11. Our study indicated that LncRNA SNGH11 can mediate the ferroptosis of liver injury cells induced by sepsis through the miR-324-3p/GPX4 axis. Suggesting that it is a new drug target for clinical treatment of sepsis and sepsis-associated liver injury, then we can improve the survival rate for sepsis patients.

ICU and Sepsis: Role of Myeloid and Lymphocyte Immune Cells.

Sepsis is a severe immune system reaction to infection and a major cause of ICU-related fatalities. Because of the high mortality, high cost of treatment, and complex aetiology of sepsis, sepsis has a huge impact on healthcare. Some of the health complications in sepsis are abnormal cardiac functions, hypoperfusion, hypotension, tissue damage, multiple organ failure, and ultimately death. Individuals with weak immune systems and chronic medical conditions are highly vulnerable to sepsis. In sepsis, a patient shows the extreme immune response in the initial stage while prolonged immunosuppression in the later stages. Sepsis-driven immunosuppression ushers in death because sepsis cases develop secondary infections postrecovery. The later immunocompromised state in sepsis is attributed myeloid-derived suppressor cell upregulation and reduced immune activity displayed by lymphocytes (lymphocyte anergy). As a result, it is currently suggested that regulating the immune response is a better therapeutic approach than focusing on inflammation to improve the immune system's capacity to fight infections. Moreover, finding novel and accurate prognostic biomarkers that can help in rapid sepsis diagnoses and deciding better therapeutic strategies will significantly lower clinical case mortality rates.

The roles, mechanism, and mobilization strategy of endogenous neural stem cells in brain injury.

Brain injury poses a heavy disease burden in the world, resulting in chronic deficits. Therapies for brain injuries have been focused on pharmacologic, small molecule, endocrine and cell-based therapies. Endogenous neural stem cells (eNSCs) are a group of stem cells which can be activated in vivo by damage, neurotrophic factors, physical factor stimulation, and physical exercise. The activated eNSCs can proliferate, migrate and differentiate into neuron, oligodendrocyte and astrocyte, and play an important role in brain injury repair and neural plasticity. The roles of eNSCs in the repair of brain injury include but are not limited to ameliorating cognitive function, improving learning and memory function, and promoting functional gait behaviors. The activation and mobilization of eNSCs is important to the repair of injured brain. In this review we describe the current knowledge of the common character of brain injury, the roles and mechanism of eNSCs in brain injury. And then we discuss the current mobilization strategy of eNSCs following brain injury. We hope that a comprehensive awareness of the roles and mobilization strategy of eNSCs in the repair of cerebral ischemia may help to find some new therapeutic targets and strategy for treatment of stroke.