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In Vivo Modeling of the Morbid Human Genome using Danio rerio

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Published on: August 24, 2013

Using ASMase knockout mice to model human diseases.

Guoqiang Hua¹, Richard Kolesnick

¹Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

Handbook of Experimental Pharmacology

|April 9, 2013

Summary

Acid sphingomyelinase (ASMase) initiates sphingomyelin/ceramide signaling, crucial for stress responses. This pathway regulates tissue injury across multiple organs, offering therapeutic intervention targets.

Area of Science:

Biochemistry
Cellular Biology
Physiology

Background:

Acid sphingomyelinase (ASMase) is a critical enzyme in sphingomyelin/ceramide signaling.
This pathway is activated by various stress stimuli and implicated in numerous diseases.
ASMase knockout mice have been instrumental in understanding its clinical relevance.

Purpose of the Study:

To review the evolutionary conservation of sphingolipid stress signaling.
To highlight mammalian adaptations in organotypic responses.
To underscore the role of ceramide generation in organ injury and fate determination.

Main Methods:

Utilizing data from ASMase knockout mouse models.
Analyzing evolutionary conservation of sphingolipid pathways.

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Reviewing literature on ceramide generation in disease states.

Main Results:

Ceramide generation by ASMase governs injury in diverse organs including tumor, gut, ovary, brain, lung, heart, and liver.
The pathway is evolutionarily conserved, with mammalian adaptations enabling organ-specific responses.
ASMase acts as a molecular switch determining tissue injury extent and organ fate.

Conclusions:

Sphingomyelin/ceramide signaling, initiated by ASMase, is a fundamental stress response pathway.
Understanding this pathway's role in organ injury is vital for therapeutic development.
Targeting ASMase offers potential for new pharmacologic interventions in various diseases.