Evidence map›Paper›PMID 41869359›Full record

ReviewFrontiers in immunology2026

Renal macrophage TLR7 signaling in lupus nephritis: from pathogenic mechanisms to therapeutic opportunities.

Longzhu Li, Zeqiong Lin, Lu Chen, Junmin Huang, Hongying Luo, Ziqian Bi, Tianyang Wang, Yongzhi Xu, Huafeng Liu, Junfeng Hao and 1 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Longzhu Li *Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, National Clinical Key Specialty Construction Program (2023), Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Zeqiong Lin *Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, National Clinical Key Specialty Construction Program (2023), Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Lu Chen *Department of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Junmin HuangDepartment of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Hongying LuoDepartment of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Ziqian BiDepartment of Computer and Information Technology, Purdue Polytechnic Institute, Purdue University, West Lafayette, IN, United States.
Tianyang WangSchool of Advanced Technology, Xi'an Jiaotong-Liverpool University, Suzhou, Jiangsu, China.
Yongzhi XuDepartment of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Huafeng LiuGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, National Clinical Key Specialty Construction Program (2023), Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Junfeng HaoDepartment of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Jiansong QiGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, National Clinical Key Specialty Construction Program (2023), Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies, including reports of rare monogenic Toll-Like Receptor 7 (TLR7) gain-of-function mutations, have established TLR7 as a causal driver in a subset of human systemic lupus erythematosus (SLE) cases. Consequently, TLR7 and its downstream mediators have emerged as promising therapeutic targets. Beyond its role in B cells, TLR7 is also critical within the renal tissue of patients with lupus nephritis (LN), where single strand RNA (ssRNA) drives aberrant TLR7 activation in macrophages. This activation promotes robust inflammatory cytokines production, exacerbating autoantigen generation and inflammatory tissue damage in a self-reinforcing feedback loop that accelerates LN progression. This review explores the role of TLR7 in LN pathogenesis through the lens of macrophage biology, with the goal of identifying novel therapeutic strategies that modulate the TLR7 signaling pathway.

Indexed as

endolysosomal TLR7 signaling blockadelupus nephritislysosomal regulationmacrophagestoll-like receptor 7

Identifiers

PMID41869359
PMCPMC12999941

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.