ReviewFrontiers in microbiology2025
Advances in molecular regulation and function of LDLR family in viral infection.
Review in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- LDLR-OPN Interaction Drives COVID-19 Myocarditis Through Monocyte Recruitment.JACC. Basic to translational science · 2026Article
- Extracellular vesicles from activated Vδ2 T cells inhibit viral replication and enhance adaptive antiviral immunity.Journal of translational medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.