Autophagy of vascular smooth muscle cells in atherosclerotic lesions

Guangdong Jia, Gang Cheng, Devendra K. Agrawal

Research output: Contribution to journalReview article

41 Scopus citations

Abstract

Autophagy genes were first identified in the yeast system and some of their mammalian orthologues have also been characterized. Increasing lines of evidence indicate that various intracellular proteins, including G proteins, mammalian target of rapamycin (mTor) and PI3K/Akt/PKB, of transmembrane signaling pathways are involved in the regulation of autophagy genes. We have recently discovered autophagy as a mechanism of cell death in atherosclerotic vascular smooth muscle cells (VSMCs). Tumor necrosis factor-α (TNF-α), insulin-like growth factor-1 (IGF-1), and 7-ketocholesterol can regulate the expression of autophagic genes, including microtubule-associated protein 1 light chain-3 (MAP1LC3) and Beclin 1, through Akt/PKB and c-jun N-terminal signal pathways in VSMCs. However, the balance between cell death and survival of VSMCs in the fibrous cap of atherosclerotic plaques appears to best correlate with plaque instability. Understanding the underlying cellular and molecular mechanisms of autophagy can provide key insights into the cell death machinery of atherosclerotic diseases.

Original languageEnglish
Pages (from-to)63-64
Number of pages2
JournalAutophagy
Volume3
Issue number1
StatePublished - Jan 2007

All Science Journal Classification (ASJC) codes

  • Cell Biology
  • Molecular Biology

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    Jia, G., Cheng, G., & Agrawal, D. K. (2007). Autophagy of vascular smooth muscle cells in atherosclerotic lesions. Autophagy, 3(1), 63-64.