The Role of ADAM17 in Inflammation-Related Atherosclerosis

Bai-Yi Tang1, Jin Ge1, Yang Wu2

  • 1Department of Cardiology, Third Xiang-Ya Hospital, Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan, China.

Insights

A disintegrin and metalloprotease 17 (ADAM17) promotes vascular inflammation, contributing to atherosclerosis development. Understanding ADAM17

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Research

Background:

  • Atherosclerosis is a chronic inflammatory disease with poor prognosis and significant economic burden.
  • A disintegrin and metalloprotease 17 (ADAM17) is a key enzyme involved in protein shedding and intracellular signaling.
  • ADAM17-mediated inflammation is implicated in atherosclerosis, but its precise role is not fully understood.

Purpose of the Study:

  • To review the activation, function, and regulation of ADAM17.
  • To detail the role of ADAM17-mediated inflammatory damage in atherosclerosis pathogenesis.
  • To discuss controversial aspects of ADAM17's involvement in atherosclerosis.

Main Methods:

  • Literature review on ADAM17 activation, function, and regulation.
  • Analysis of ADAM17's role in inflammatory processes within vascular cells.
  • Synthesis of current knowledge on ADAM17 and atherosclerosis.

Main Results:

  • ADAM17 promotes vascular inflammation in endothelial cells, smooth muscle cells, and macrophages.
  • ADAM17 plays a regulatory role in the occurrence and development of atherosclerosis.
  • The specific mechanisms linking ADAM17's diverse functions to atherosclerosis pathogenesis require further elucidation.

Conclusions:

  • ADAM17 is a significant mediator of vascular inflammation contributing to atherosclerosis.
  • Further insights into ADAM17 biology may facilitate rational management strategies for atherosclerosis.
  • Targeting ADAM17 could offer a potential therapeutic avenue for preventing and treating atherosclerosis.

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