Evidence map›Paper›PMID 35821117›Full record

ArticleCell discovery2022

Single-cell atlas of keratoconus corneas revealed aberrant transcriptional signatures and implicated mechanical stretch as a trigger for keratoconus pathogenesis.

Shengqian Dou, Qun Wang, Bin Zhang, Chao Wei, Huijin Wang, Ting Liu, Haoyun Duan, Hui Jiang, Mingna Liu, Xiaolin Qi and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
12.8field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026
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  15. Studies of mice with a large deletion of the ARPKD-associatedbioRxiv : the preprint server for biology · 2026
    Article
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Shengqian Dou *Eye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Qun Wang *Eye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Bin ZhangEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Chao WeiEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Huijin WangEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Ting LiuEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Haoyun DuanEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Hui JiangEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Mingna LiuEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Xiaolin QiEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Qingjun ZhouEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Lixin XieEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China.
Weiyun ShiEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China. wyshi@sdfmu.edu.cn.
Hua GaoEye Institute of Shandong First Medical University, State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Qingdao, Shandong, China. hgao@sdfmu.edu.cn.
Shandong Eye Hospital · CNShandong First Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81800876National Natural Science Foundation of China (National Science Foundation of China) 81870639National Natural Science Foundation of China (National Science Foundation of China) 82070923Taishan Scholar Foundation of Shandong Province 20150215Taishan Scholar Foundation of Shandong Province 201812150
6 · The paper itself

Abstract

Keratoconus is a common ectatic corneal disorder in adolescents and young adults that can lead to progressive visual impairment or even legal blindness. Despite the high prevalence, its etiology is not fully understood. In this study, we performed single-cell RNA sequencing (scRNA-Seq) analysis on 39,214 cells from central corneas of patients with keratoconus and healthy individuals, to define the involvement of each cell type during disease progression. We confirmed the central role of corneal stromal cells in this disease, where dysregulation of collagen and extracellular matrix (ECM) occurred. Differential gene expression and histological analyses revealed two potential novel markers for keratoconus stromal cells, namely CTSD and CTSK. Intriguingly, we detected elevated levels of YAP1 and TEAD1, the master regulators of biomechanical homeostasis, in keratoconus stromal cells. Cyclical mechanical experiments implicated the mechanical stretch in prompting protease production in corneal stromal cells during keratoconus progression. In the epithelial cells of keratoconus corneas, we observed reduced basal cells and abnormally differentiated superficial cells, unraveling the corneal epithelial lesions that were usually neglected in clinical diagnosis. In addition, several elevated cytokines in immune cells of keratoconus samples supported the involvement of inflammatory response in the progression of keratoconus. Finally, we revealed the dysregulated cell-cell communications in keratoconus, and found that only few ligand-receptor interactions were gained but a large fraction of interactional pairs was erased in keratoconus, especially for those related to protease inhibition and anti-inflammatory process. Taken together, this study facilitates the understanding of molecular mechanisms underlying keratoconus pathogenesis, providing insights into keratoconus diagnosis and potential interventions.

Identifiers

PMID35821117
PMCPMC9276680
OpenAlexW4285036105

What OpenQuestion holds

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Registered trials

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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.