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Acute kidney injury to chronic kidney disease transition: insufficient cellular stress response.

Publication ,  Journal Article
Strausser, SA; Nakano, D; Souma, T
Published in: Curr Opin Nephrol Hypertens
July 2018

PURPOSE OF REVIEW: Recent epidemiological and preclinical mechanistic studies provide strong evidence that acute kidney injury (AKI) and chronic kidney disease (CKD) form an interconnected syndrome. Injured kidneys undergo a coordinated reparative process with an engagement of multiple cell types after injury; however, maladaptation to the injury subjects kidneys to a vicious cycle of fibrogenesis and nephron loss. In this review, we will outline and discuss the pathogenesis of AKI-to-CKD transition with an emphasis on dysregulated 'cellular stress adaptation' as a potential therapeutic target. RECENT FINDINGS: Recent studies identify the crucial role of injured tubular epithelial cells in the transition from AKI to CKD. Damaged tubular cells undergo reactivation of developmental and epithelial-mesenchymal transition signaling, metabolic alteration, and cell-cycle arrest, thereby driving inflammation and fibrogenesis. Recent work highlights that cellular stress-adaptive pathways against hypoxic and oxidative stress provide insufficient protection after severe AKI episode. SUMMARY: Insufficient cellular stress adaptation may underpin the persistent activation of inflammatory and fibrogenic signaling in damaged kidneys. We propose that harnessing cellular stress-adaptive responses will be a promising therapeutic strategy to halt or even reverse the deleterious process of AKI-to-CKD transition.

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Published In

Curr Opin Nephrol Hypertens

DOI

EISSN

1473-6543

Publication Date

July 2018

Volume

27

Issue

4

Start / End Page

314 / 322

Location

England

Related Subject Headings

  • Urology & Nephrology
  • Signal Transduction
  • Renal Insufficiency, Chronic
  • Oxidative Stress
  • NF-E2-Related Factor 2
  • Kidney Tubules
  • Kidney
  • Kelch-Like ECH-Associated Protein 1
  • Humans
  • Fibrosis
 

Citation

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Strausser, S. A., Nakano, D., & Souma, T. (2018). Acute kidney injury to chronic kidney disease transition: insufficient cellular stress response. Curr Opin Nephrol Hypertens, 27(4), 314–322. https://doi.org/10.1097/MNH.0000000000000424
Strausser, Sarah A., Daisuke Nakano, and Tomokazu Souma. “Acute kidney injury to chronic kidney disease transition: insufficient cellular stress response.Curr Opin Nephrol Hypertens 27, no. 4 (July 2018): 314–22. https://doi.org/10.1097/MNH.0000000000000424.
Strausser SA, Nakano D, Souma T. Acute kidney injury to chronic kidney disease transition: insufficient cellular stress response. Curr Opin Nephrol Hypertens. 2018 Jul;27(4):314–22.
Strausser, Sarah A., et al. “Acute kidney injury to chronic kidney disease transition: insufficient cellular stress response.Curr Opin Nephrol Hypertens, vol. 27, no. 4, July 2018, pp. 314–22. Pubmed, doi:10.1097/MNH.0000000000000424.
Strausser SA, Nakano D, Souma T. Acute kidney injury to chronic kidney disease transition: insufficient cellular stress response. Curr Opin Nephrol Hypertens. 2018 Jul;27(4):314–322.

Published In

Curr Opin Nephrol Hypertens

DOI

EISSN

1473-6543

Publication Date

July 2018

Volume

27

Issue

4

Start / End Page

314 / 322

Location

England

Related Subject Headings

  • Urology & Nephrology
  • Signal Transduction
  • Renal Insufficiency, Chronic
  • Oxidative Stress
  • NF-E2-Related Factor 2
  • Kidney Tubules
  • Kidney
  • Kelch-Like ECH-Associated Protein 1
  • Humans
  • Fibrosis