Evidence map›Paper›PMID 34142044›Full record

ArticleiScience2021

Macrophage recruitment in immune-privileged lens during capsule repair, necrotic fiber removal, and fibrosis.

Yuting Li, Zhen Li, Yumeng Quan, Hongyun Cheng, Manuel A Riquelme, Xiao-Dong Li, Sumin Gu, Jean X Jiang

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
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

12 citing papers in PubMed, 17 citations in OpenAlex.

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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

8 authors at 1 institution in 2 countries.

Yuting LiDepartment of Ophthalmology, Lanzhou University Second Hospital, Lanzhou, Gansu 730000, China.
Zhen LiDepartment of Biochemistry and Structural Biology and, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Yumeng QuanDepartment of Biochemistry and Structural Biology and, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Hongyun ChengDepartment of Biochemistry and Structural Biology and, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Manuel A RiquelmeDepartment of Biochemistry and Structural Biology and, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Xiao-Dong LiDepartment of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Sumin GuDepartment of Biochemistry and Structural Biology and, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Jean X JiangDepartment of Biochemistry and Structural Biology and, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Intercellular Communication in the Eye LensR01EY012085 · NEI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Jean X Jiang · 2003 to 2026
$8.4M
NEI NIH HHS R01 EY012085
6 · The paper itself

Abstract

Emerging evidence challenges the lens as an immune-privileged organ. Here, we provide a direct mechanism supporting a role of macrophages in lens capsule rupture repair. Posterior lens capsule rupture in a connexin 50 and aquaporin 0 double-knockout mouse model resulted in lens tissue extrusion into the vitreous cavity with formation of a "tail-like" tissue containing delayed regressed hyaloid vessels, fibrotic tissue and macrophages at postnatal (P) 15 days. The macrophages declined after P 30 days with M2 macrophages detected inside the lens. By P 90 days, the "tail-like" tissue completely disappeared and the posterior capsule rupture was sealed with thick fibrotic tissue. Colony-stimulating factor 1 (CSF-1) accelerated capsule repair, whereas inhibition of the CSF-1 receptor delayed the repair. Together, these results suggest that lens posterior rupture leads to the recruitment of macrophages delivered by the regression delayed hyaloid vessels. CSF-1-activated M2 macrophages mediate capsule rupture repair and development of fibrosis.

Indexed as

ImmunologyOphthalmology

Identifiers

PMID34142044
PMCPMC8188486
OpenAlexW3160370600

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.