Potential biochemical mechanisms of lung injury in diabetes

Hong Zheng, Jinzi Wu, Zhen Jin, Liang Jun Yan

Research output: Contribution to journalReview article

15 Scopus citations

Abstract

Accumulating evidence has shown that the lung is one of the target organs for microangiopathy in patients with either type 1 or type 2 diabetes mellitus (DM). Diabetes is associated with physiological and structural abnormalities in the diabetic lung concurrent with attenuated lung function. Despite intensive investigations in recent years, the pathogenic mechanisms of diabetic lung injury remain largely elusive. In this review, we summarize currently postulated mechanisms of diabetic lung injury. We mainly focus on the pathogenesis of diabetic lung injury that implicates key pathways, including oxidative stress, non-enzymatic protein glycosylation, polyol pathway, NF-?B pathway, and protein kinase c pathway. We also highlight that while numerous studies have mainly focused on tissue or cell damage in the lung, studies focusing on mitochondrial dysfunction in the diabetic lung have remained sketchy. Hence, further understanding of mitochondrial mechanisms of diabetic lung injury should provide invaluable insights into future therapeutic approaches for diabetic lung injury.

Original languageEnglish
Pages (from-to)7-16
Number of pages10
JournalAging and Disease
Volume8
Issue number1
DOIs
StatePublished - 1 Jan 2017

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Keywords

  • Diabetes mellitus
  • Diabetic hyperglycemia
  • Diabetic lung injury
  • Mitochondria
  • Oxidative stress

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