Phospholipid Membrane Transport and Associated Diseases

Phospholipids are the basic structure block of eukaryotic membranes, in both the outer and inner membranes, which delimit cell organelles. Phospholipids can also be damaged by oxidative stress produced by mitochondria, for instance, becoming oxidized phospholipids. These damaged phospholipids have b...

Full description

Saved in:
Bibliographic Details
Published inBiomedicines Vol. 10; no. 5; p. 1201
Main Authors Ventura, Raúl, Martínez-Ruiz, Inma, Hernández-Alvarez, María Isabel
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 23.05.2022
MDPI
Subjects
Online AccessGet full text
ISSN2227-9059
2227-9059
DOI10.3390/biomedicines10051201

Cover

More Information
Summary:Phospholipids are the basic structure block of eukaryotic membranes, in both the outer and inner membranes, which delimit cell organelles. Phospholipids can also be damaged by oxidative stress produced by mitochondria, for instance, becoming oxidized phospholipids. These damaged phospholipids have been related to prevalent diseases such as atherosclerosis or non-alcoholic steatohepatitis (NASH) because they alter gene expression and induce cellular stress and apoptosis. One of the main sites of phospholipid synthesis is the endoplasmic reticulum (ER). ER association with other organelles through membrane contact sites (MCS) provides a close apposition for lipid transport. Additionally, an important advance in this small cytosolic gap are lipid transfer proteins (LTPs), which accelerate and modulate the distribution of phospholipids in other organelles. In this regard, LTPs can be established as an essential point within phospholipid circulation, as relevant data show impaired phospholipid transport when LTPs are defected. This review will focus on phospholipid function, metabolism, non-vesicular transport, and associated diseases.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
These authors contributed equally to this work.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines10051201