We demonstrated firstly that during fibrosis development, there is a net decrease in macrophage phagocytosis since the macrophage population with high phagocytic ability in fibrotic conditions (F4/80low−CD11b+) decreases during the progression of fibrosis while the macrophage population with low phagocytic ability (F4/80high−CD11b+) increases during the progression of fibrosis; and secondly, that macrophage-CPT1a cell therapy with a high phagocytic ability is associated with a therapeutic effect on kidney fibrosis. Here, CPT1A is linked to fibrosis.