PDF(Pubmed)
Abstract：
Diabetic kidney disease (DKD) is a leading cause of end stage renal disease with unmet clinical demands for treatment. Lipids are essential for cell survival; however, renal cells have limited capability to metabolize overloaded lipids. Dyslipidaemia is common in DKD patients and renal ectopic lipid accumulation is associated with disease progression. Unveiling the molecular mechanism involved in renal lipid regulation is crucial for exploring potential therapeutic targets. In this review, we focused on the mechanism underlying cholesterol, oxysterol and fatty acid metabolism disorder in the context of DKD. Specific regulators of lipid accumulation in different kidney compartment and TREM2 macrophages, a lipid-related macrophages in DKD, were discussed. The role of sodium-glucose transporter 2 inhibitors in improving renal lipid accumulation was summarized.
摘要：
糖尿病肾病（DKD）是终末期肾病的主要原因，临床治疗需求未得到满足。脂质是细胞存活所必需的；然而，肾细胞代谢超负荷脂质的能力有限。血脂异常在DKD患者中很常见，肾脏异位脂质积累与疾病进展有关。揭示参与肾脏脂质调节的分子机制对于探索潜在的治疗靶点至关重要。在这次审查中,我们专注于胆固醇的潜在机制，氧化固醇和脂肪酸代谢紊乱在DKD的背景下。不同肾区和TREM2巨噬细胞中脂质积累的特定调节剂，DKD中脂质相关的巨噬细胞，进行了讨论。总结了钠-葡萄糖转运蛋白2抑制剂在改善肾脏脂质积累中的作用。
