Sphingomyelin is a type of sphingolipid found in membranes, especially in the membranous myelin sheath that surrounds some nerve cell axons. 

Sphingomyelins can also be classified as sphingophospholipids.

In humans, SPH represents ~85% of all sphingolipids, and typically make up 10–20 mol % of plasma membrane lipids.

Sphingomyelin content in mammals ranges from 2 to 15% in most tissues, with higher concentrations found in nerve tissues, red blood cells, and the ocular lenses. 

Sphingomyelin has significant structural and functional roles in the cell. 

Sphingomyelin is a plasma membrane component and participates in many signaling pathways. 

Sphingomyelin consists of a phosphocholine head group, a sphingosine, and a fatty acid. 

The sphingosine and fatty acid can collectively be categorized as a ceramide. 

This composition-ceramide- allows sphingomyelin to play significant roles in signaling pathways.

The degradation and synthesis of sphingomyelin produce important second messengers for signal transduction.

Sphingomyelin obtained from natural sources, such as eggs contains fatty acids of various chain length. 

Sphingomyelin is available commercially.

Sphingomyelin undergoes significant interactions with cholesterol. 

Sphingomyelin is synthesized at the endoplasmic reticulum (ER), where it can be found in low amounts, and at the trans Golgi. 

It is enriched at the plasma membrane.

It has a greater concentration on the outer than the inner leaflet of the plasma membrane.

The Golgi complex represents an intermediate between the endoplasmic reticulum and plasma membrane.

Sphingomyelin synthesis involves the enzymatic transfer of a phosphocholine from phosphatidylcholine to a ceramide. 

The ceramide is transported to the Golgi apparatus where it can be converted to sphingomyelin by sphingomyelin synthase 

Sphingomyelin breakdown is responsible for initiating many universal signaling pathways. 

It is hydrolyzed by sphingomyelinases.

Nerve cell axon membranous myelin sheaths are rich in sphingomyelin, suggesting its role as an electrical insulator of nerve fibers.

The plasma membrane of other cells is also abundant in sphingomyelin, largely in the exoplasmic leaflet of the cell membrane. 

Sphingomyelin plays a significant role in cell signaling pathways. 

The synthesis of sphingomyelin at the plasma membrane by sphingomyelin synthase 2 produces diacylglycerol.

Diacylglycerol is a lipid-soluble second messenger that can pass along a signal cascade. 

The degradation of sphingomyelin can produce ceramide which is involved in the apoptotic signaling pathway.

Sphingomyelin hydrolysis and ceramide signaling are essential in the decision of whether a cell dies. 

Sphingomyelin, and other sphingolipids, are associated with lipid microdomains in the plasma membrane known as lipid rafts. 

Lipid rafts are characterized by the lipid molecules offering more structure and rigidity compared to the rest of the plasma membrane, and are thought to be involved in many cell processes, such as membrane sorting and trafficking, signal transduction, and cell polarization.

Excessive sphingomyelin in lipid rafts may lead to insulin resistance.

Lipid rafts have been speculated to be involved in the cascade of cell apoptosis.

Sphingomyelin can accumulate in a hereditary disease called Niemann–Pick disease.

It is a genetically-inherited disease caused by a deficiency in the lysosomal enzyme acid sphingomyelinase, which causes the accumulation of sphingomyelin in spleen, liver, lungs, bone marrow, and brain, causing irreversible neurological damage. 

In the autoimmune disease multiple sclerosis (MS), the myelin sheath of neuronal cells in the brain and spinal cord is degraded, resulting in loss of signal transduction capability. 

The activation of sphingomyelinase, an enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide; sphingomyelinase activity has been observed in conjunction with cellular apoptosis.

An excess of sphingomyelin in the red blood cell membrane, as occurs in abetalipoproteinemia, causes excess lipid accumulation in the outer leaflet of the red blood cell plasma membrane, resulting in abnormally shaped red cells called acanthocytes.

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