Division of Nephrology, Department of Medicine, School of Medicine, University of Connecticut Health Center, Farmington, CT 06030-1405, USA.
Department of Immunology, School of Medicine, University of Connecticut Health Center, Farmington, CT 06030-1405, USA.
Cells. 2023 Jun 8;12(12):1584. doi: 10.3390/cells12121584.
Kidney disease is a significant health problem worldwide, affecting an estimated 10% of the global population. Kidney disease encompasses a diverse group of disorders that vary in their underlying pathophysiology, clinical presentation, and outcomes. These disorders include acute kidney injury (AKI), chronic kidney disease (CKD), glomerulonephritis, nephrotic syndrome, polycystic kidney disease, diabetic kidney disease, and many others. Despite their distinct etiologies, these disorders share a common feature of immune system dysregulation and metabolic disturbances. The immune system and metabolic pathways are intimately connected and interact to modulate the pathogenesis of kidney diseases. The dysregulation of immune responses in kidney diseases includes a complex interplay between various immune cell types, including resident and infiltrating immune cells, cytokines, chemokines, and complement factors. These immune factors can trigger and perpetuate kidney inflammation, causing renal tissue injury and progressive fibrosis. In addition, metabolic pathways play critical roles in the pathogenesis of kidney diseases, including glucose and lipid metabolism, oxidative stress, mitochondrial dysfunction, and altered nutrient sensing. Dysregulation of these metabolic pathways contributes to the progression of kidney disease by inducing renal tubular injury, apoptosis, and fibrosis. Recent studies have provided insights into the intricate interplay between immune and metabolic pathways in kidney diseases, revealing novel therapeutic targets for the prevention and treatment of kidney diseases. Potential therapeutic strategies include modulating immune responses through targeting key immune factors or inhibiting pro-inflammatory signaling pathways, improving mitochondrial function, and targeting nutrient-sensing pathways, such as mTOR, AMPK, and SIRT1. This review highlights the importance of the interplay between immune and metabolic pathways in kidney diseases and the potential therapeutic implications of targeting these pathways.
肾病是全球范围内一个重大的健康问题，影响着全球约 10%的人口。肾病涵盖了一组不同的疾病，其在潜在病理生理学、临床表现和结果方面存在差异。这些疾病包括急性肾损伤 (AKI)、慢性肾脏病 (CKD)、肾小球肾炎、肾病综合征、多囊肾病、糖尿病肾病等。尽管这些疾病的病因不同，但它们都有一个共同的特点，即免疫系统失调和代谢紊乱。免疫系统和代谢途径密切相关，相互作用以调节肾脏疾病的发病机制。在肾脏疾病中，免疫反应的失调包括各种免疫细胞类型（包括固有和浸润免疫细胞）、细胞因子、趋化因子和补体因子之间的复杂相互作用。这些免疫因素可以引发和持续肾脏炎症，导致肾组织损伤和进行性纤维化。此外，代谢途径在肾脏疾病的发病机制中起着关键作用，包括葡萄糖和脂质代谢、氧化应激、线粒体功能障碍和营养感应改变。这些代谢途径的失调通过诱导肾小管损伤、细胞凋亡和纤维化，促进肾脏疾病的进展。最近的研究揭示了免疫和代谢途径在肾脏疾病中的复杂相互作用，为肾脏疾病的预防和治疗提供了新的治疗靶点。潜在的治疗策略包括通过靶向关键免疫因子或抑制促炎信号通路来调节免疫反应、改善线粒体功能以及靶向营养感应途径，如 mTOR、AMPK 和 SIRT1。本综述强调了免疫和代谢途径在肾脏疾病中的相互作用的重要性以及靶向这些途径的潜在治疗意义。
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