The Role of Scavenger Receptors in Health and Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (30 April 2026) | Viewed by 813

Special Issue Editors


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Guest Editor
1. Cell Biology, Neurosciences and Experimental Myology Laboratory, Victor Babeș Institute of Pathology, 050096 Bucharest, Romania
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
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Guest Editor
1. Department of Cellular and Molecular Biology and Histology, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
2. “Victor Babeș” 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, scavenger receptors have arisen as a key participant in the multiplayer environment of different homeostatic and diseased states and as a brilliant example of resource optimization in a biological system.

Scavenger receptors (SRs) are a heterogeneous group of membrane-bound receptors that recognize and internalize a wide range of ligands, including modified lipoproteins, pathogens, and cellular debris. There are many types of scavenger receptors with diverse biological activities—such as SR-A (SR-A1, MARCO), LOX-1 (SR-E1), SR-B1 (SCARB1), and CXCL16 (SR-PSOX). Among them, CD36 (SR-B2) has been extensively studied for its multifaceted functions.

In homeostatic conditions, CD36 is expressed by a wide variety of cell types, where it supports various functions. It was introduced as a cell adhesion molecule on platelets and erythrocytes with a 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).

Inhibiting CD36 or LOX-1 could mitigate atherosclerosis and cancer progression, while enhancing SR-B1 activity may improve cholesterol metabolism. Meanwhile, SR-A and MARCO modulation could influence infectious disease outcomes. Given their roles in lipid metabolism, inflammation, and pathogen clearance, scavenger receptors are promising therapeutic targets.

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
Prof. Dr. Mihail E. Hinescu
Guest Editors

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Keywords

  • scavenger receptor
  • CD36
  • lipid scavenger
  • cell-to-matrix adhesion
  • metastasis
  • neoangiogenesis
  • biomarker

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Published Papers (1 paper)

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Research

24 pages, 5678 KB  
Article
Different Functions of Human Scavenger Receptors BI and BII Overexpressed in a Murine Abdominal Sepsis Model
by Naoki Hayase, Tatyana G. Vishnyakova, Irina N. Baranova, Alexander V. Bocharov, Xuzhen Hu, Amy P. Patterson, Peter S. T. Yuen, Thomas L. Eggerman and Robert A. Star
Biomolecules 2026, 16(5), 670; https://doi.org/10.3390/biom16050670 - 1 May 2026
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Abstract
Class B scavenger receptor BI splice variants (SR-BI) and BII (SR-BII) internalize lipoproteins but also bind and internalize bacteria. Their individual roles in sepsis are unknown. We overexpressed human SR-BI or BII in transgenic mice, primarily in the liver, but also in the [...] Read more.
Class B scavenger receptor BI splice variants (SR-BI) and BII (SR-BII) internalize lipoproteins but also bind and internalize bacteria. Their individual roles in sepsis are unknown. We overexpressed human SR-BI or BII in transgenic mice, primarily in the liver, but also in the kidney and in bone marrow-derived macrophages, and then performed cecal ligation and puncture (CLP) surgery. SR-BI and BII transgenic mice had significantly worse survival compared to WT mice. Twenty-four hours after CLP, liver injury markers and histological damage were elevated in both SR-BI and BII transgenic mice, whereas kidney damage was similar. Systemic inflammatory cytokines were markedly increased in SR-BI and BII transgenic mice; parallel increases were seen in liver mRNA expression, but not in the kidney. The highest degree of neutrophil infiltration was observed in the liver of SR-BI. Human SR-BI and BII dramatically decreased bacterial accumulation in the liver. Green fluorescent protein-labeled E. coli were efficiently phagocytosed in hepatic macrophages of SR-BI and BII transgenic mice; phagocytosis was more prominent in SR-BII transgenic mice. Finally, human SR-BI overexpression reduced systemic HDL-C levels, eliminated adrenal cortex lipid droplets, and dampened the systemic increase of corticosterone after CLP. Supplementation with glucocorticoid and mineralocorticoid improved survival in SR-BI but not in SR-BII transgenic mice after CLP. In summary, our findings suggest human SR-BI and BII overexpression contributes to higher mortality after CLP by different mechanisms: excessive inflammatory response due to adrenal insufficiency (SR-BI) or hyperactive phagocytosis (SR-BII) in the liver. Full article
(This article belongs to the Special Issue The Role of Scavenger Receptors in Health and Disease)
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