Inflammation response

炎症反应
  • 文章类型: Journal Article
    BMP和活化素膜结合抑制剂(BAMBI)是一种跨膜糖蛋白,被称为TGFβ的假受体,as,虽然它的胞外结构域与I型TGFβ受体相似,其细胞内结构较短,缺乏丝氨酸/苏氨酸磷酸激酶信号基序。BAMBI可以调节许多生物学现象,包括葡萄糖和脂质代谢,炎症反应,细胞增殖和分化。此外,BAMBI在mRNA和蛋白质水平的异常表达有助于各种人类病理,包括肥胖和癌症.在本次审查中,简要介绍了BAMBI的结构,描述了其相关的信号通路和生理功能。了解BAMBI结构和功能可能有助于了解疾病的发生,包括肥胖和糖尿病,在其他人中。本综述为BAMBI作为潜在的生物标志物或治疗靶点的开发提供了理论基础。
    BMP and activin membrane-bound inhibitor (BAMBI) is a transmembrane glycoprotein, known as a pseudo-receptor for TGFβ, as, while its extracellular domain is similar to that of type I TGFβ receptors, its intracellular structure is shorter and lacks a serine/threonine phosphokinase signaling motif. BAMBI can regulate numerous biological phenomena, including glucose and lipid metabolism, inflammatory responses, and cell proliferation and differentiation. Furthermore, abnormal expression of BAMBI at the mRNA and protein levels contributes to various human pathologies, including obesity and cancer. In the present review, the structure of BAMBI is briefly introduced and its associated signaling pathways and physiological functions are described. Understanding of BAMBI structure and function may contribute to knowledge regarding the occurrence of diseases, including obesity and diabetes, among others. The present review provides a theoretical foundation for the development of BAMBI as a potential biomarker or therapeutic target.
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  • 文章类型: Journal Article
    急性胰腺炎(AP),作为临床急腹症的常见原因,往往导致多器官损伤。在严重AP的过程中,除了胰腺,肺和肠是最容易受影响的器官。这些器官损害相继发生。值得注意的是,肺和肠道损伤密切相关。对ML的损害,它运输免疫细胞,肠液,Chyle,和有毒成分(包括毒素,胰蛋白酶,和激活的细胞因子到AP中的体循环)可以连接到AP。这一过程可导致肺高渗水肿的病理变化,肺泡液水平升高,肠粘膜结构的破坏,肠粘膜通透性受损。肺和肠损伤相关的潜在机制是炎症反应,氧化应激,和内分泌激素分泌紊乱。肺和肠损伤的主要信号通路是TNF-α,HMGB1介导的NF-κB信号通路的炎症扩增效应,Nrf2/ARE氧化应激反应信号通路,和IL-6介导的JAK2/STAT3信号通路。这些途径发挥抗炎反应和抗氧化应激,抑制细胞增殖,促进细胞凋亡。这种相互作用符合中医关于肺与大肠相连的理论(中文为飞宇达昌翔标利)。本文旨在探讨AP中肺和肠损伤的交叉机制,以开发新的治疗策略。
    Acute pancreatitis (AP), as a common cause of clinical acute abdomen, often leads to multi-organ damage. In the process of severe AP, the lungs and intestines are the most easily affected organs aside the pancreas. These organ damages occur in succession. Notably, lung and intestinal injuries are closely linked. Damage to ML, which transports immune cells, intestinal fluid, chyle, and toxic components (including toxins, trypsin, and activated cytokines to the systemic circulation in AP) may be connected to AP. This process can lead to the pathological changes of hyperosmotic edema of the lung, an increase in alveolar fluid level, destruction of the intestinal mucosal structure, and impairment of intestinal mucosal permeability. The underlying mechanisms of the correlation between lung and intestinal injuries are inflammatory response, oxidative stress, and endocrine hormone secretion disorders. The main signaling pathways of lung and intestinal injuries are TNF-α, HMGB1-mediated inflammation amplification effect of NF-κB signal pathway, Nrf2/ARE oxidative stress response signaling pathway, and IL-6-mediated JAK2/STAT3 signaling pathway. These pathways exert anti-inflammatory response and anti-oxidative stress, inhibit cell proliferation, and promote apoptosis. The interaction is consistent with the traditional Chinese medicine theory of the lung being connected with the large intestine (fei yu da chang xiang biao li in Chinese). This review sought to explore intersecting mechanisms of lung and intestinal injuries in AP to develop new treatment strategies.
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