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Renal lipotoxicity: Insights from experimental models
Clinical and Experimental Pharmacology and Physiology ( IF 2.4 ) Pub Date : 2021-07-27 , DOI: 10.1111/1440-1681.13556 Barbara Bruna Abreu Castro 1, 2 , Orestes Foresto-Neto 3 , Niels Olsen Saraiva-Camara 3 , Helady Sanders-Pinheiro 1, 2
Clinical and Experimental Pharmacology and Physiology ( IF 2.4 ) Pub Date : 2021-07-27 , DOI: 10.1111/1440-1681.13556 Barbara Bruna Abreu Castro 1, 2 , Orestes Foresto-Neto 3 , Niels Olsen Saraiva-Camara 3 , Helady Sanders-Pinheiro 1, 2
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In recent decades, there has been a progressive increase in the prevalence of obesity and chronic kidney disease. Renal lipotoxicity has been associated with obesity. Although lipids play fundamental physiological roles, the accumulation of lipids in kidney cells may cause dysfunction and/or renal fibrosis. Adipose tissue that exceeds their lipid storage capacity begins to release triglycerides into the bloodstream that can get stored in several organs, including the kidneys. The mechanisms underlying renal lipotoxicity involve intracellular lipid accumulation and organelle dysfunction, which trigger oxidative stress and inflammation that consequently result in insulin resistance and albuminuria. However, the specific pathways involved in renal lipotoxicity have not yet been fully understood. We aimed to summarize the current knowledge on the mechanisms by which lipotoxicity affects the renal morphology and function in experimental models of obesity. The accumulation of fatty acids in tubular cells has been described as the main mechanism of lipotoxicity; however, lipids and their metabolism also affect the function and the survival of podocytes. In this review, we presented indication of mitochondrial, lysosomal and endoplasmic reticulum alterations involved in kidney damage caused by obesity. The kidney is vulnerable to lipotoxicity, and studies of the mechanisms underlying renal injury caused by obesity can help identify therapeutic targets to control renal dysfunction.
中文翻译：
肾脂毒性：实验模型的见解
近几十年来，肥胖和慢性肾病的患病率逐渐增加。肾脂毒性与肥胖有关。尽管脂质发挥着基本的生理作用，但脂质在肾细胞中的积累可能导致功能障碍和/或肾纤维化。超过其脂质储存能力的脂肪组织开始将甘油三酯释放到血液中，这些甘油三酯可以储存在包括肾脏在内的多个器官中。肾脂毒性的机制涉及细胞内脂质积累和细胞器功能障碍，从而引发氧化应激和炎症，从而导致胰岛素抵抗和蛋白尿。然而，涉及肾脂毒性的具体途径尚未完全了解。我们的目的是总结目前关于脂毒性影响肥胖实验模型中肾脏形态和功能的机制的知识。脂肪酸在肾小管细胞中的积累被描述为脂毒性的主要机制；然而，脂质及其代谢也会影响足细胞的功能和存活。在这篇综述中，我们提出了线粒体、溶酶体和内质网改变与肥胖引起的肾脏损伤有关的迹象。肾脏容易受到脂毒性的影响，对肥胖引起的肾损伤机制的研究有助于确定控制肾功能障碍的治疗靶点。
更新日期：2021-07-27
中文翻译：
肾脂毒性：实验模型的见解
近几十年来，肥胖和慢性肾病的患病率逐渐增加。肾脂毒性与肥胖有关。尽管脂质发挥着基本的生理作用，但脂质在肾细胞中的积累可能导致功能障碍和/或肾纤维化。超过其脂质储存能力的脂肪组织开始将甘油三酯释放到血液中，这些甘油三酯可以储存在包括肾脏在内的多个器官中。肾脂毒性的机制涉及细胞内脂质积累和细胞器功能障碍，从而引发氧化应激和炎症，从而导致胰岛素抵抗和蛋白尿。然而，涉及肾脂毒性的具体途径尚未完全了解。我们的目的是总结目前关于脂毒性影响肥胖实验模型中肾脏形态和功能的机制的知识。脂肪酸在肾小管细胞中的积累被描述为脂毒性的主要机制；然而，脂质及其代谢也会影响足细胞的功能和存活。在这篇综述中，我们提出了线粒体、溶酶体和内质网改变与肥胖引起的肾脏损伤有关的迹象。肾脏容易受到脂毒性的影响，对肥胖引起的肾损伤机制的研究有助于确定控制肾功能障碍的治疗靶点。
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