The Role of CD36 in Human Health and Disease
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".
Deadline for manuscript submissions: 31 August 2025 | Viewed by 2657
Special Issue Editors
2. Department of Cellular and Molecular Biology and Histology, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania
Interests: prognostic markers; cancer biomarkers; cancer biology
2. "Victor Babes" National Institute of Pathology, 050096 Bucharest, Romania
Interests: prognostic markers; cancer biomarkers; cancer biology; cancer metastasis; metastasis
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
During recent years, the CD36 receptor has arisen as a key participant in the multiplayer environment of different homeostatic and diseased states and a brilliant example of resource optimisation in a biological system.
In homeostatic conditions, CD36 is expressed by a wide varety of cell types, where it supports various functions. It was introduced as a cell adhesion molecule on platelets and erythrocytes with high affinity for collagens and thrombospondin-1, but later on, it was found to support many other roles, from the recognition, uptake, and processing of fatty acids, to lipids scavenging for anionic or oxidized phospholipids or lipoproteins, angiogenesis inhibition by impairing endothelial cell migration and promoting apoptosis, microglial binding and the clearance of hydrophobic amyloid fibrils in brains affected by Alzheimer’s disease, and even the recognition and clearance of fungi and bacteria, just to name a few. As a result, it has acquired many names along the way, from glycoprotein IV (GPIV) to fatty acid translocase (FAT), scavenger receptor class B (SR-B2), or glycoprotein 88 (GP88).
There are also multiple CD36-related mechanisms for promoting cancer progression and metastasis, mostly in relation to trombospondins. Other studies suggested that the induction of CD36 expression on tumour cells shifts metabolism from glucose oxidation to lipid uptake and storage, and is proportional to their metastatic potential or cancer progression through epithelial–mesenchymal transition (EMT).
This Special Issue is an open invitation to highlight what is already demonstrated and to encourage going beyond the edges of this already-expanding universe.
Dr. Laura Cristina Ceafalan
Dr. Mihail E. Hinescu
Guest Editors
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Keywords
- CD36
- lipid scavenger
- cell-to-matrix adhesion
- metastasis
- neoangiogenesis
- biomarker
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