Martínez-Hernández Sandra Luz, Muñoz-Ortega Martín Humberto, Ávila-Blanco Manuel Enrique, Medina-Pizaño Mariana Yazmin, Ventura-Juárez Javier
Departamento de Microbiología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes 20100, Ags, Mexico.
Departamento de Química, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes 20100, Ags, Mexico.
Biomedicines. 2023 Oct 18;11(10):2828. doi: 10.3390/biomedicines11102828.
Chronic kidney disease (CKD) is characterized by renal parenchymal damage leading to a reduction in the glomerular filtration rate. The inflammatory response plays a pivotal role in the tissue damage contributing to renal failure. Current therapeutic options encompass dietary control, mineral salt regulation, and management of blood pressure, blood glucose, and fatty acid levels. However, they do not effectively halt the progression of renal damage. This review critically examines novel therapeutic avenues aimed at ameliorating inflammation, mitigating extracellular matrix accumulation, and fostering renal tissue regeneration in the context of CKD. Understanding the mechanisms sustaining a proinflammatory and profibrotic state may offer the potential for targeted pharmacological interventions. This, in turn, could pave the way for combination therapies capable of reversing renal damage in CKD. The non-replacement phase of CKD currently faces a dearth of efficacious therapeutic options. Future directions encompass exploring vaptans as diuretics to inhibit water absorption, investigating antifibrotic agents, antioxidants, and exploring regenerative treatment modalities, such as stem cell therapy and novel probiotics. Moreover, this review identifies pharmaceutical agents capable of mitigating renal parenchymal damage attributed to CKD, targeting molecular-level signaling pathways (TGF-β, Smad, and Nrf2) that predominate in the inflammatory processes of renal fibrogenic cells.
慢性肾脏病(CKD)的特征是肾实质损伤导致肾小球滤过率降低。炎症反应在导致肾衰竭的组织损伤中起关键作用。目前的治疗选择包括饮食控制、矿物质盐调节以及血压、血糖和脂肪酸水平的管理。然而,它们并不能有效阻止肾损伤的进展。本综述批判性地研究了旨在改善炎症、减轻细胞外基质积累并促进CKD背景下肾组织再生的新型治疗途径。了解维持促炎和促纤维化状态的机制可能为靶向药物干预提供潜力。这反过来又可能为能够逆转CKD肾损伤的联合疗法铺平道路。CKD的非替代阶段目前面临有效治疗选择匮乏的问题。未来的方向包括探索作为利尿剂的血管加压素受体拮抗剂以抑制水吸收、研究抗纤维化药物、抗氧化剂以及探索再生治疗方式,如干细胞疗法和新型益生菌。此外,本综述确定了能够减轻CKD所致肾实质损伤的药物,这些药物靶向在肾成纤维细胞炎症过程中占主导地位的分子水平信号通路(TGF-β、Smad和Nrf2)。