PPARGC1A and diabetic kidney disease: Yanrong Lu et al. investigated the mechanisms underlying MSC’s improved mitochondrial function in macrophages (M2) [121] and found that transferring mitochondria from MSCs to macrophages reduced inflammation and reduced kidney injury in a mouse model of diabetic nephropathy by promoting mitochondrial biogenesis via regulating the transcription of PPARGC1A or PGC-1α and clearing out damaged cells via PGC-1/TFEB mediated autophagy [122].