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Updated: Jan 11, 2026
LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring
Published on: November 17, 2018
Advances in molecular regulation and function of LDLR family in viral infection
Qing Yao1,2, Jun Gong1, Helin Lu1
1School of Pharmacy, Hubei University of Science and Technology, Xianning, China.
Abstract:
The low-density lipoprotein receptor (LDLR) family represents a crucial interface between cellular cholesterol homeostasis and viral pathogenesis. This review systematically examines the dual roles of these receptors in viral infections, encompassing both their well-established function as entry receptors for various viruses and their emerging role as regulators of viral replication through lipid metabolic pathways. The LDLR family mediates exogenous cholesterol uptake that supports viral proliferation while simultaneously suppressing endogenous cholesterol synthesis. This suppression triggers endoplasmic reticulum cholesterol depletion, which activates the STING-TBK1 signaling axis, thereby establishing a potent antiviral state. These opposing mechanisms reveal the complex involvement of the LDLR family in viral infections. This article aims to synthesize current understanding of these processes and explore the translational potential of targeting the LDLR-lipid-virus axis for developing novel antiviral strategies, while acknowledging the challenges in selectively modulating these dual functions for therapeutic purposes.
Insights
The low-density lipoprotein receptor (LDLR) family plays a dual role in viral infections, acting as entry points and regulating viral replication via lipid metabolism. Targeting this axis offers potential for new antiviral therapies.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- The low-density lipoprotein receptor (LDLR) family is critical for cellular cholesterol balance.
- These receptors are increasingly recognized for their involvement in viral pathogenesis.
- Their roles extend beyond viral entry to regulating viral replication through lipid metabolism.
Purpose of the Study:
- To systematically review the dual roles of the LDLR family in viral infections.
- To synthesize current understanding of LDLR-mediated lipid metabolism in viral replication.
- To explore therapeutic potential targeting the LDLR-lipid-virus axis.
Main Methods:
- Systematic literature review.
- Analysis of LDLR function in viral entry.
- Examination of LDLR's role in lipid metabolism and antiviral signaling.
Main Results:
- LDLR family members serve as entry receptors for numerous viruses.
- They mediate exogenous cholesterol uptake, supporting viral proliferation.
- Suppression of endogenous cholesterol synthesis by LDLRs triggers an antiviral state via the STING-TBK1 pathway.
Conclusions:
- The LDLR family exhibits complex, opposing roles in viral infections.
- Targeting the LDLR-lipid-virus axis presents novel antiviral strategy potential.
- Challenges exist in selectively modulating LDLR functions for therapeutic benefit.
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