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Impairment of calcium ATPases by high glucose and potential pharmacological protection

L Horáková1, M K Strosova, C M Spickett

  • 1Institute of Experimental Pharmacology and Toxicology, SAS, Bratislava, Slovakia. exfahorl@savba.sk

Free Radical Research
|May 29, 2013
PubMed

Insights

High glucose impairs Ca(2+)-ATPases through oxidative stress and glycation, leading to calcium imbalance and diabetic complications. This review explores prevention strategies for Ca(2+)-pump glycation.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Background:

  • Elevated glucose levels are linked to oxidative stress and cellular dysfunction.
  • Calcium ATPases (Ca(2+)-ATPases) play crucial roles in maintaining calcium homeostasis.
  • Dysfunctional Ca(2+)-ATPases are implicated in diabetes and its chronic complications.

Purpose of the Study:

  • To review the impairment of Ca(2+)-ATPases by high glucose and its derivatives.
  • To explore the mechanisms linking glucose, oxidative stress, glycation, and Ca(2+)-ATPase dysfunction.
  • To discuss potential strategies for preventing Ca(2+)-pump glycation.

Main Methods:

  • Literature review of in vitro studies, human diabetes data, and experimental animal models.
  • Analysis of biochemical pathways involving glucose metabolism, oxidative stress, and protein modification.
  • Examination of structural and functional alterations in Ca(2+)-ATPases.

Main Results:

  • High glucose induces oxidative stress, directly impacting Ca(2+)-ATPase function.
  • Non-enzymatic glycation of Ca(2+)-ATPases, particularly at the ATP binding domain, alters their structure and function.
  • Glycation can progress from reversible to irreversible advanced glycation end products (AGEs), affecting cysteine-674.
  • Ca(2+) imbalance resulting from Ca(2+)-ATPase dysfunction contributes to diabetic complications.

Conclusions:

  • Impaired Ca(2+)-ATPases due to high glucose and glycation are key contributors to diabetic pathophysiology.
  • Understanding glycation sites and mechanisms is crucial for developing therapeutic interventions.
  • Further research into prevention strategies for Ca(2+)-pump glycation is warranted.

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