来自高血压和肥胖小鼠的细胞获得炎症,衰老和衰老的表型
Sierra R McKinzie1, Natalya Kaverina1, Robert Allen Schweickart2
1Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington, United States.
American journal of physiology. Renal physiology
|February 29, 2024
概括
高血压和肥胖在小鼠中加快了细胞衰老和炎症. 这些条件诱导与压力相关的衰老和无菌炎症,影响脏健康.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 分子生物学分子生物学
- 老年学是一门学科.
背景情况:
- 高血压和肥胖是导致球功能障碍的主要原因.
- 细胞损伤和枯竭有助于脏疾病的进展.
研究的目的:
- 为了研究高血压和肥胖症下的细胞中的分子变化.
- 为了确定与 podocyte 功能障碍相关的转录性改变.
主要方法:
- 在年轻小鼠中,通过使用脱氧皮质乙酸盐 (DOCA) 诱导的高血压和通过高脂肪饮食 (HFD) 诱导的肥胖.
- 在孤立的 podocytes 上进行了批量 mRNA 测序.
- 使用免疫染验证了关键发现.
主要成果:
- 高血压和肥胖模型都显示了 kanonical podocyte 蛋白和 podocyte 数量的降低.
- 细胞表现出无菌炎症,由NLRP3炎症体,PD-1和TLR通路的增加表明.
- 细胞显示了衰老和衰老基因的表达增加,包括与衰老相关的分泌表现型.
- 高血压相关的衰老包括与年龄相关的标志物 (p16,p19),而肥胖显示压力诱导的标志物 (p21,p53).
结论:
- 足细胞衰老,衰老和炎症在实验性高血压和肥胖症中至关重要.
- 加快的 podocyte 衰老和无菌炎症有助于淋巴细胞功能障碍.
- 在高血压中,不同的衰老途径被激活,而肥胖引起的细胞损伤则被激活.
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