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When apoptosis meets autophagy: deciding cell fate after trauma and sepsis

Journal

TRENDS IN MOLECULAR MEDICINE
Volume 15, Issue 3, Pages 129-138

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2009.01.002

Keywords

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Funding

  1. National Institutes of Health (NIH) National Institute of Environmental Health Sciences (NIEHS) [R01 ES015323]
  2. NIH National Institute of General Medical Sciences (NIGMS) [R37 39519, RO1 GM39519]
  3. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES015323] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R37GM039519, R01GM037127, R01GM039519] Funding Source: NIH RePORTER

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Apoptotic cell death is considered to be an underlying mechanism in immunosuppression and multiple organ dysfunction after trauma-hemorrhage and sepsis. Although studied intensively over the last decade, the role of other cell death mechanisms under similar pathophysiological conditions has remained elusive. Recently, autophagy has emerged as an important mediator of programmed cell death pathways. Here, we review recent advances in our understanding of apoptosis and autophagy and the crosstalk between these processes. We explore the coexistence of these two processes and the effects of autophagy on apoptosis after trauma-hemorrhage and sepsis. The inter-relationship between autophagy and apoptosis might unveil novel therapeutic approaches for the detection and treatment of trauma-hemorrhage and sepsis.

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