Fig. 1: DKD is associated with increased expression of PVT1 and mitochondria damage.

A Levels of PVT1 in the plasma and kidney tissues from controls and patients with DKD. B The correlation between PVT1 levels and UACR (r = 0.535, P < 0.01) or Scr (r = 0.318, P = 0.029). C RNA-FISH combined with immunofluorescence illustrated the distribution of PVT1 and its relative position to podocin by confocal laser scanning microscope (n = 3). The podocytes were labeled with arrows. D Levels of Pvt1 in the kidney tissues from CTL mice and STZ mice at 6 weeks (n = 7), 8 weeks (n = 7), 12 weeks (n = 7), and 20 weeks (n = 5) after the onset of diabetes. E RNA-FISH combined with immunofluorescence illustrated the distribution of Pvt1 and its relative position to podocin in paraffin-embedded mouse sections by confocal laser scanning microscope (n = 5). The podocytes were labeled with arrows. F PAS staining of glomeruli from CTL mice and STZ mice at 20 weeks after DKD initiation (n = 5). G TEM image of podocytes, GBM, and mitochondria in primary podocytes from CTL mice and STZ mice at 20 weeks after DKD initiation (n = 5). H Measurement of the mitochondrial OCR of primary podocytes from CTL mice and STZ mice at 20 weeks after DKD initiation (n = 5). I Energy phenotype profile (EPP) was mentioned. J Relative mRNA levels of Tfam and mitochondrial OXPHOS genes in CTL mice and STZ mice at 20 weeks after DKD initiation (n = 5). K Relative mRNA levels of proinflammatory cytokines (Il-6, Tnf-α, Cxcl10, and Icam1) in CTL mice and STZ mice at 20 weeks after DKD initiation (n = 5). L ELISA showed the levels of TNF-α in the plasma from healthy subjects (n = 25) and clinical patients with DKD (n = 47). Error bars represent the mean± S.D, *P < 0.05, **P < 0.01, and ***P < 0.001.