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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Cell Signal. 2020 Jun 20;73:109698. doi: 10.1016/j.cellsig.2020.109698

Table 2.

Evidences in support for the role of IGF-1 pathway in pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).

Study ADPKD model Findings
1 Nakamura et al. 1993 [35] DBA/2FG-pcy mice

  • Increase in IGF-1 mRNA
2 Aukema et al. 2001 [36] Han:SPRD-cy rat

  • IGF-1 levels higher in cy/+

  • Dietary soy protein delays the disease progression
3 Parker et al. 2007 [38] Conditional immortalized cystic cells

  • IGF-1 induces hyperproliferation via ras/raf pathway
4 Song et al. 2009 [37] Cysts of different sizes and minimally cystic tissue from human ADPKD kidney

  • Upregulation of IGF-1/IGFR1
5 Liu et al. 2013 (39)[170] Immortalized epithelial cells from ADPKD patients

  • Rosiglitazone inhibits IGF-1-induced cyst lining epithelial cell proliferation
6 Warner et al. 2016 [40] Pkd1RC/RC mice

  • Food restriction reduced the serum IGF-1 levels

  • Food restriction also reduced renal Igf 1 mRNA expression.
7 Kashyap et al. 2020 [41] Human ADPKD kidney tissue sections and cystic fluids, 9–12 ADPKD tubular epithelial cells,
Pkd1RC/RC, Pkd2WS25/−, Pkd1RC/RC-Pappa mutant mice and metanephros

  • PAPP-A significantly higher in human and experimental ADPKD

  • PAPP-A genetic deficiency as well as antibody treatment ameliorates the cystic disease.