Chronic kidney disease (CKD), defined as persistent (>3 months) kidney functional loss, has a growing prevalence (>10% worldwide population) and limited treatment options. Fibrosis driven by the aberrant accumulation of extracellular matrix is the final common pathway of nearly all types of chronic repetitive injury in the kidney and is considered a hallmark of CKD. Myofibroblasts are key extracellular matrix-producing cells that are activated by crosstalk between damaged tubules and immune cells. Emerging evidence indicates that metabolic alterations are crucial contributors to the pathogenesis of kidney fibrosis by affecting cellular bioenergetics and metabolite signalling. Immune cell functions are intricately connected to their metabolic characteristics, and kidney cells seem to undergo cell-type-specific metabolic shifts in response to damage, all of which can determine injury and repair responses in CKD. A detailed understanding of the heterogeneity in metabolic reprogramming of different kidney cellular subsets is essential to elucidating communication processes between cell types and to enabling the development of metabolism-based innovative therapeutic strategies against CKD.

慢性肾病 (CKD) 被定义为持续性（>3 个月）肾功能丧失，其患病率不断上升（>10% 全球人口），且治疗选择有限。由细胞外基质异常积累驱动的纤维化是几乎所有类型的肾脏慢性重复性损伤的最终共同途径，被认为是 CKD 的标志。肌成纤维细胞是关键的细胞外基质生成细胞，可通过受损小管和免疫细胞之间的串扰激活。新的证据表明，代谢改变通过影响细胞生物能和代谢信号传导，是肾纤维化发病机制的关键因素。免疫细胞功能与其代谢特征密切相关，肾细胞似乎会因损伤而发生细胞类型特异性的代谢变化，所有这些都可以决定 CKD 中的损伤和修复反应。详细了解不同肾细胞亚群代谢重编程的异质性对于阐明细胞类型之间的通讯过程以及开发基于代谢的创新治疗策略至关重要。