Responses to Ang II (Angiotensin II), Salt Intake, and Lipopolysaccharide Reveal the Diverse Actions of TNF-α (Tumor Necrosis Factor-α) on Blood Pressure and Renal Function.
Responses to Ang II (Angiotensin II), Salt Intake, and Lipopolysaccharide Reveal the Diverse Actions of TNF-α (Tumor Necrosis Factor-α) on Blood Pressure and Renal Function.
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对Ang II（血管紧张素II）、盐摄入量和脂多糖的反应揭示了TNF-α（肿瘤坏死因子-α）对血压和肾功能的不同作用。
DOI：
10.1161/hypertensionaha.122.19464
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发表时间：
2022-12
期刊：
影响因子：
8.3
通讯作者：
Ferreri, Nicholas R.
中科院分区：
文献类型：
--
作者：
Crorkin, Patrick;Hao, Shoujin;Ferreri, Nicholas R.
肿瘤坏死因子-α是一种促炎细胞因子，但该细胞因子也具有重要的免疫调节和调节功能。随着肿瘤坏死因子-α对免疫系统功能影响的揭示，在研究人员确定肿瘤坏死因子-α促进宿主防御和慢性炎症的环境和机制之前，其活性谱似乎相互矛盾。这些影响反映了自我保护机制，当调控失调时，这种机制可能会变得有害。自那以后，在肺、结肠和肾脏中发现了肿瘤坏死因子-α的生理和病理生理效应的范例，在肺、结肠和肾脏中，已经分别确定了它在肺水肿、电解质重吸收和血压调节中的作用。最近关于肿瘤坏死因子-α在心血管系统中的促高血压和炎症作用的研究，以及与氯化钠和血压稳态相关的研究，肾脏对内毒素的反应，以及对细菌感染的保护，正在帮助确定肿瘤坏死因子-α调节肾脏内不同功能的机制。本文讨论了肾上皮细胞产生肿瘤坏死因子-α的调节机制，该调节机制不仅调节电解质排泄和血压动态平衡，而且维持适当的局部高盐度环境，以优化肾脏对细菌感染的先天性免疫反应。肿瘤坏死因子-α介导的广泛效应可能与疾病的严重程度、炎症程度、肿瘤坏死因子-α水平以及产生这种细胞因子的特定细胞类型有关，这些方面仍有待进一步研究。
Tumor necrosis factor-alpha (TNF-α) is best known as a pro-inflammatory cytokine, yet this cytokine also has important immunomodulatory and regulatory functions. As the effects of TNF-α on immune system function were being revealed, the spectrum of its activities appeared in conflict with each other before investigators defined the settings and mechanisms by which TNF-α contributed to both host defense and chronic inflammation. These effects reflect self-protective mechanisms that may become harmful when dysregulated. The paradigm of physiological and pathophysiological effects of TNF-α has since been uncovered in the lung, colon, and kidney where its role has been identified in pulmonary edema, electrolyte reabsorption, and blood pressure regulation, respectively. Recent studies on the pro-hypertensive and inflammatory effects of TNF-α in the cardiovascular system juxtaposed to those related to NaCl and blood pressure homeostasis, the response of the kidney to lipopolysaccharide, and protection against bacterial infections are helping define the mechanisms by which TNF-α modulates distinct functions within the kidney. This review discusses how production of TNF-α by renal epithelial cells may contribute to regulatory mechanisms that not only govern electrolyte excretion and blood pressure homeostasis but also maintain the appropriate local hypersalinity environment needed for optimizing the innate immune response to bacterial infections in the kidney. It is possible that the wide range of effects mediated by TNF-α may be related to severity of disease, amount of inflammation and TNF-α levels, and the specific cell types that produce this cytokine, areas that remain to be investigated further.