Journal
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
Volume 53, Issue 3, Pages 198-208Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e31819b52d5
Keywords
apoptosis; mitochondria; ceramide synthase; LASS (Cer-S); sphingomyelinase; cytochrome c; Bax; PP2A; cathepsin D; Bcl-2
Funding
- NIH/NCCR [P20 RR 17677-04]
- VA Merit award
- NIH [AG16583]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR017677] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG016583] Funding Source: NIH RePORTER
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A hallmark of tissue injury in various models of ischemia/reperfusion (IR) is mitochondrial dysfunction and the release of mitochondrial proapoptotic proteins leading to cell death. Although IR-induced mitochondrial injury has been extensively Studied and key mitochondrial functions affected by IR are chiefly characterized, the nature of the molecule that causes loss of mitochondrial integrity and function remains obscure. It has become increasingly clear that ceramide, a membrane sphingolipid and a key mediator of cell stress responses, could play a critical role in IR-induced mitochondrial damage. Emerging data point to excessive ceramide accumulation in tissue and, specifically, ill mitochondria after IR. Exogenously added to isolated mitochondria, ceramide could mimic sonic of the mitochondrial dysfunctions Occurring ill IR. The recent identification and characterization of major enzymes in ceramide synthesis is expected to contribute to the understanding of molecular mechanisms of ceramide involvement in mitochondrial damage in IR. This review will examine the experimental evidence supporting the important role of ceramide in mitochondrial dysfunction in IR to highlight potential targets for pharmacological manipulation of ceramide levels.
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