MiR‐182 inhibits kidney fibrosis by regulating transforming growth factor β1/Smad3 pathway in autosomal dominant polycystic kidney disease

IUBMB Life ◽  
2020 ◽  
Vol 72 (7) ◽  
pp. 1340-1348
Author(s):  
Liping Sun ◽  
Chaofeng Hu ◽  
Zhen Wang ◽  
Xinzhou Zhang
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Polycystic Kidney ◽  
Kidney Fibrosis ◽  
Autosomal Dominant Polycystic Kidney

scholarly journals Hepatic Production of Fibroblast Growth Factor 23 in Autosomal Dominant Polycystic Kidney Disease

2018 ◽  
Vol 103 (6) ◽  
pp. 2319-2328 ◽  
Author(s):  
Frank Bienaimé ◽  
Ariane Ambolet ◽  
Béatrice Aussilhou ◽  
François Brazier ◽  
Marie Fouchard ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Polycystic Kidney Disease ◽  
Plasma Levels ◽  
Autosomal Dominant ◽  
Fibroblast Growth ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Cystic Liver

Abstract Context The bone-derived hormone fibroblast growth factor (FGF) 23 controls phosphate homeostasis and urinary phosphate excretion. FGF23 plasma levels increase in the early stage of renal insufficiency to prevent hyperphosphatemia. Recent evidence suggests that this increase has effects on cardiac and immune cells that compromise patients’ health. Patients with autosomal dominant polycystic kidney disease (ADPKD) have been reported to have higher FGF23 concentrations than other patients with similar renal function. The significance of this finding has remained unknown. Methods and Results Analyzing the FGF23 plasma levels in 434 patients with ADPKD and 355 control subjects with a measured glomerular filtration rate (mGFR) between 60 and 120 mL/min per 1.73 m2, we confirmed that patients with ADPKD had higher FGF23 plasma concentrations than controls. Remarkably, this difference did not translate into renal phosphate leakage. Using different assays for FGF23, we found that this discrepancy was explained by a predominant increase in the cleaved C-terminal fragment of FGF23, which lacks phosphaturic activity. We found that FGF23 plasma concentration independently correlated with the severity of cystic liver disease in ADPKD. We observed that, in contrast to control liver tissues, the cystic liver from patients with ADPKD markedly expressed FGF23 messenger RNA and protein. In line with this finding, the surgical reduction of polycystic liver mass was associated with a decrease in FGF23 plasma levels independently of any modification in mGFR, phosphate, or iron status. Conclusion Our findings demonstrate that severely polycystic livers produce FGF23 and increase levels of circulating FGF23 in patients with ADPKD.

scholarly journals The Controversial Role of Fibrosis in Autosomal Dominant Polycystic Kidney Disease

2020 ◽  
Vol 21 (23) ◽  
pp. 8936
Author(s):  
Maria Fragiadaki ◽  
Fiona M. Macleod ◽  
Albert C. M. Ong
Keyword(s):  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Transforming Growth Factor Beta ◽  
Autosomal Dominant ◽  
Transforming Growth Factor ◽  
Kidney Diseases ◽  
Janus Kinase ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is characterized by the progressive growth of cysts but it is also accompanied by diffuse tissue scarring or fibrosis. A number of recent studies have been published in this area, yet the role of fibrosis in ADPKD remains controversial. Here, we will discuss the stages of fibrosis progression in ADPKD, and how these compare with other common kidney diseases. We will also provide a detailed overview of some key mechanistic pathways to fibrosis in the polycystic kidney. Specifically, the role of the ‘chronic hypoxia hypothesis’, persistent inflammation, Transforming Growth Factor beta (TGFβ), Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) and microRNAs will be examined. Evidence for and against a pathogenic role of extracellular matrix during ADPKD disease progression will be provided.

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