Skeletal muscle is one of the largest organs in the body and the largest protein repository. Mitochondria are the main energy-producing organelles in cells and play an important role in skeletal muscle health and function. They participate in several biological processes related to skeletal muscle metabolism, growth, and regeneration. Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor and regulator of systemic energy balance. AMPK is involved in the control of energy metabolism by regulating many downstream targets. In this review, we propose that AMPK directly controls several facets of mitochondrial function, which in turn controls skeletal muscle metabolism and health. This review is divided into four parts. First, we summarize the properties of AMPK signal transduction and its upstream activators. Second, we discuss the role of mitochondria in myogenesis, muscle atrophy, regeneration post-injury of skeletal muscle cells. Third, we elaborate the effects of AMPK on mitochondrial biogenesis, fusion, fission and mitochondrial autophagy, and discuss how AMPK regulates the metabolism of skeletal muscle by regulating mitochondrial function. Finally, we discuss the effects of AMPK activators on muscle disease status. This review thus represents a foundation for understanding this biological process of mitochondrial dynamics regulated by AMPK in the metabolism of skeletal muscle. A better understanding of the role of AMPK on mitochondrial dynamic is essential to improve mitochondrial function, and hence promote skeletal muscle health and function.
Primary Ewing's sarcoma (ES) is rare, especially when it occurs in the spinal canal during middle or old age. The rarity of Ewing's sarcoma breakpoint region 1 fusion-negative ES has been reported in the literature. The present case report describes a 60-year-old Chinese patient who was diagnosed with ES originating from the spinal canal in 2016. The patient was hospitalized with pain resembling electric shock in the waist and buttocks, which occurred intermittently for 1 month, and incontinence for 1 week. Magnetic resonance imaging demonstrated multiple inhomogeneous, oval-shaped nodules in the intradural and cauda equina spaces of T12-L3. The largest nodule was ~23×11×10 mm. The patient underwent right adrenal tumour resection. A histopathologic examination of the focal area revealed that the tumour consisted of small, circular haematoxylin stained cells that formed typical Homer-Wright rosettes. Immunohistochemical analysis confirmed that the patient suffered from ES due to positive staining for membranous cluster of differentiation 99 (CD99), cytokeratin (CK) and nuclear foetal-liver infusion 1 (FLI-1). In conclusion, the histopathological presence of Homer-Wright rosettes and immunohistochemical markers such as CD99, FLI-1 and CK are valuable factors for the diagnosis of ES, although cytogenetic analysis is considered the gold standard. Complete surgery is the most effective treatment option for ES treatment. Adjuvant radiotherapy and combination chemotherapy can also improve the survival rate of patients postoperatively.
Background: Sepsis is a condition of organ dysfunction caused by infection, and is unavoidably related to costs and mortality; however, no biomarker has yet been identified to clearly predict the prognosis of septic patients. In this study, we aimed to explore the role of guanine-rich sequence factor 1 (GRSF1) in evaluating the severity and prognosis of sepsis.
Methods:The expression of GRSF1 in peripheral blood was measured and analyzed in 42 septic participants and 32 healthy controls respectively by using quantitative reverse transcription polymerase chain reaction (RT-qPCR). Clinical data were assessed by correlation analysis. In addition, GRSF1 expression was investigated in cecal ligation and puncture (CLP) induced mice septic models by RT-qPCR and western blot (WB).
Results:The expression of GRSF1 expression in septic patients in the first day of electronic intensive care unit (eICU) administration was significantly lower in comparison with HC. Further analysis showed GRSF1 expression was strongly related to the Acute Physiologic Assessment and Chronic Health Evaluation II (APACHE II) score and Sequential Organ Failure Assessment (SOFA) score. Low expression of GRSF1 predicted high mortality within 24 hours in septic patients and in CLP-induced mice.Conclusions: Decreased expression of GRSF1 was significantly correlated with high mortality in septic patients, and also in experimental septic mice. The GRSF1 protein may be a potential prognostic biomarker in sepsis.
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