Autophagy as a novel therapeutic target in vascular calcification

Kanchan Phadwal, Du Feng, Dongxing Zhu, Victoria MacRae

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

The autophagy pathway is a key regulator of cellular metabolism and homeostasis, and plays a critical role in maintaining normal vascular cell function. It is well recognized that autophagy can regulate endothelial cell homeostasis, vascular smooth muscle cell (VSMC) phenotype transition, and calcium (Ca2+) homeostasis in VSMCs. Emerging evidence has demonstrated that autophagy directly protects against vascular calcification (VC). Crosstalk between endosomes, dysfunctional mitochondria, autophagic vesicles and Ca2+ and phosphate (Pi) enriched matrix vesicles (MVs) may underpin the pathogenesis of VC. In this review, we summarize the current experimental evidence in understanding how autophagy maintains normal vascular cell function and its protective role against vascular calcification. We also discuss the underlying molecular and cellular mechanisms through which autophagy inhibits vascular calcification. Pharmacological modulation of autophagy may offer an exciting new strategy for the treatment of vascular calcification
Original languageEnglish
JournalPharmacology and Therapeutics
Early online date21 Oct 2019
Publication statusE-pub ahead of print - 21 Oct 2019

Keywords / Materials (for Non-textual outputs)

  • Autophagy
  • Vascular cell function
  • Phenotype transition
  • Matrix vesicles
  • Vascular calcification


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