Cross talk between autophagy and apoptosis in pulmonary hypertension

Research output: Contribution to journalReview article

25 Scopus citations

Abstract

Endothelial cell (EC) apoptosis and apoptosis resistant proliferation have been proposed to play crucial roles in the development of featured plexiform lesions in the pathogenesis of pulmonary hypertension (PH). Subsequently, EC injury associated smooth muscle cell (SMC) proliferation facilitates vascular remodeling and eventually leads to narrowed vascular lumen, increased pulmonary vascular resistance, increased pulmonary arterial pressure, and right heart failure. The imbalance between cell death and proliferation occurs in every stage of pulmonary vascular remodeling and pathogenesis of PH, and involves every cell type in the vasculature including, but not limited to ECs, SMCs, and fibroblasts. Despite extensive studies, the detailed cellular and molecular mechanisms on how the transition from initial apoptosis of ECs to apoptosis resistant proliferation on ECs and SMCs remains unclear. Recent knowledge on autophagy, a conservative and powerful regulatory machinery existing in almost all mammalian cells, has shed light on the complex and delicate control on cell fate in the development of vascular remodeling in PH. In this review, we will discuss the recent understandings on how the cross-talk between apoptosis and autophagy regulates cell death or proliferation in PH pathogenesis, particularly in pulmonary vascular remodeling involving ECs and SMCs.

Original languageEnglish (US)
Pages (from-to)407-414
Number of pages8
JournalPulmonary Circulation
Volume2
Issue number4
DOIs
StatePublished - Oct 2012

Keywords

  • Apoptosis
  • Autophagy
  • Beclin-1
  • LC3
  • Pulmonary hypertension

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Fingerprint Dive into the research topics of 'Cross talk between autophagy and apoptosis in pulmonary hypertension'. Together they form a unique fingerprint.

Cite this