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Assessment of Vascular Function in Patients With Chronic Kidney Disease
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Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

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The endoplasmic reticulum stress and the unfolded protein response in kidney disease: Implications for vascular

Carlo Alberto Ricciardi1, Luigi Gnudi1

  • 1King's College of London, Faculty of Life Sciences & Medicine, School of Cardiovascular Medicine & Sciences, Section Vascular Biology and Inflammation, British Heart Foundation Centre for Research Excellence, London, UK.

Journal of Cellular and Molecular Medicine
|October 17, 2020
PubMed

Insights

Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) are key in kidney disease. Understanding these pathways may reveal new therapeutic targets for acute kidney injury (AKI) and chronic kidney disease (CKD).

Area of Science:

  • Nephrology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Acute kidney injury (AKI) and chronic kidney disease (CKD) pose significant healthcare challenges.
  • Effective therapies for kidney diseases are limited, necessitating novel biomarkers and pharmacological targets.
  • Endoplasmic reticulum (ER) stress is increasingly recognized for its role in kidney disease pathophysiology.

Purpose of the Study:

  • To review the cellular response to ER stress, including the unfolded protein response (UPR) pathways (PERK, IRE1α, ATF6).
  • To examine the interplay between ER and mitochondria in kidney disease.
  • To discuss the link between renal injury mediators, particularly vascular growth factors, and ER stress/UPR in AKI and CKD, identifying potential therapeutic targets.

Main Methods:

  • Literature review focusing on cellular mechanisms of ER stress and UPR in kidney disease.
  • Analysis of the interplay between ER and mitochondria.
  • Examination of the relationship between vascular growth factors and ER stress in renal pathophysiology.

Main Results:

  • ER stress, activated by cellular insults, triggers the UPR.
  • The UPR involves major branches: PERK, IRE1α, and ATF6.
  • ER-mitochondria crosstalk is crucial in the pathophysiology of kidney diseases.

Conclusions:

  • ER stress and UPR are central to AKI and CKD pathogenesis.
  • Targeting ER stress and UPR pathways, along with their interaction with mitochondria and growth factors, offers promising avenues for novel kidney disease therapies.
Keywords:
Endoplasmic reticulum stressacute kidney injurychronic kidney diseaseunfolded protein responsevascular growth factors

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