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Hepatic dysfunction after spinal cord injury: A vicious cycle of central and peripheral pathology?
Experimental Neurology ( IF 5.3 ) Pub Date : 2019-12-18 , DOI: 10.1016/j.expneurol.2019.113160
Matthew T Goodus 1 , Dana M McTigue 1
Affiliation  

The liver is essential for numerous physiological processes, including filtering blood from the intestines, metabolizing fats, proteins, carbohydrates and drugs, and regulating iron storage and release. The liver is also an important immune organ and plays a critical role in response to infection and injury throughout the body. Liver functions are regulated by autonomic parasympathetic innervation from the brainstem and sympathetic innervation from the thoracic spinal cord. Thus, spinal cord injury (SCI) at or above thoracic levels disrupts major regulatory mechanisms for hepatic functions. Work in rodents and humans shows that SCI induces liver pathology, including hepatic inflammation and fat accumulation characteristic of a serious form of non-alcoholic fatty liver disease (NAFLD) called non-alcoholic steatohepatitis (NASH). This hepatic pathology is associated with and likely contributes to indices of metabolic dysfunction often noted in SCI individuals, such as insulin resistance and hyperlipidemia. These occur at greater rates in the SCI population and can negatively impact health and quality of life. In this review, we will: 1) Discuss acute and chronic changes in human and rodent liver pathology and function after SCI; 2) Describe how these hepatic changes affect systemic inflammation, iron regulation and metabolic dysfunction after SCI; 3) Describe how disruption of the hepatic autonomic nervous system may be a key culprit in post-injury chronic liver pathology; and 4) Preview ongoing and future research that aims to elucidate mechanisms driving liver and metabolic dysfunction after SCI.

中文翻译:

脊髓损伤后的肝功能不全:中枢和周围病理的恶性循环?

肝脏对于许多生理过程至关重要,包括从肠中过滤血液,代谢脂肪,蛋白质,碳水化合物和药物,以及调节铁的储存和释放。肝脏也是重要的免疫器官,在整个人体对感染和伤害的反应中起着至关重要的作用。肝功能由脑干的自主性副交感神经支配和胸脊髓的交感神经支配来调节。因此,胸水平或以上的脊髓损伤(SCI)破坏了肝功能的主要调节机制。在啮齿动物和人类中进行的研究表明,SCI可诱发肝脏病理,包括肝脏炎症和严重的非酒精性脂肪肝病(NAFLD)形式的脂肪积累,这种疾病称为非酒精性脂肪性肝炎(NASH)。这种肝病理与SCI个体经常注意到的代谢功能障碍指标有关,并可能促成该指标的异常,例如胰岛素抵抗和高脂血症。这些在SCI人群中的发生率更高,并且可能对健康和生活质量产生负面影响。在这篇综述中,我们将:1)讨论SCI后人类和啮齿动物肝脏病理和功能的急性和慢性变化;2)描述这些肝脏变化如何影响SCI后的全身炎症,铁调节和代谢功能障碍;3)描述肝自主神经系统的破坏如何成为受伤后慢性肝病理的关键元凶;和4)预览正在进行的和未来的研究,旨在阐明SCI后驱动肝脏和代谢功能障碍的机制。
更新日期:2019-12-19
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