Phosphatidylethanolamine (PE) is a key phospholipid component of biological membranes, especially within the inner mitochondrial membrane. Scientific research has established that PE plays a vital role in mitochondrial structure, dynamics, and function. The synthesis and maintenance of PE are crucial for the assembly of mitochondrial respiratory chain complexes, which are essential for ATP production and cellular energy metabolism. Mutations or deficiencies in enzymes involved in PE biosynthesis, such as phosphatidylserine decarboxylase, have been linked to impaired mitochondrial function and even mitochondrial-associated diseases in animal models and humans.

Experimental studies in yeast, mice, and cell cultures have shown that lowering PE levels can cause mitochondrial dysfunction, including defective oxidative phosphorylation and structural abnormalities in mitochondria. Supplementation or genetic restoration of PE biosynthesis can reverse some of these defects. While direct human supplementation studies with phosphatidylethanolamine targeting mitochondrial health are limited, the biochemical and genetic evidence from model systems provides moderate scientific support for its role in maintaining mitochondrial integrity.

Nevertheless, more clinical trials are needed to confirm whether oral or supplemental PE can significantly benefit mitochondrial function in humans. Current evidence supports its importance in mitochondrial biology, but translational data for supplementation are still emerging.