Single-cell RNA-seq reveals fibroblast heterogeneity and increased mesenchymal fibroblasts in human fibrotic skin diseases

Cheng-Cheng Deng, Yong-Fei Hu, Ding-Heng Zhu, Qing Cheng, Jing-Jing Gu, Qing-Lan Feng, Li-Xue Zhang, Ying-Ping Xu, Dong Wang, Zhili Rong () and Bin Yang ()
Additional contact information
Cheng-Cheng Deng: Dermatology Hospital, Southern Medical University
Yong-Fei Hu: Dermatology Hospital, Southern Medical University
Ding-Heng Zhu: Dermatology Hospital, Southern Medical University
Qing Cheng: Dermatology Hospital, Southern Medical University
Jing-Jing Gu: Dermatology Hospital, Southern Medical University
Qing-Lan Feng: Dermatology Hospital, Southern Medical University
Li-Xue Zhang: Dermatology Hospital, Southern Medical University
Ying-Ping Xu: Dermatology Hospital, Southern Medical University
Dong Wang: Dermatology Hospital, Southern Medical University
Zhili Rong: Dermatology Hospital, Southern Medical University
Bin Yang: Dermatology Hospital, Southern Medical University

Nature Communications, 2021, vol. 12, issue 1, 1-16

Abstract: Abstract Fibrotic skin disease represents a major global healthcare burden, characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix. Fibroblasts are found to be heterogeneous in multiple fibrotic diseases, but fibroblast heterogeneity in fibrotic skin diseases is not well characterized. In this study, we explore fibroblast heterogeneity in keloid, a paradigm of fibrotic skin diseases, by using single-cell RNA-seq. Our results indicate that keloid fibroblasts can be divided into 4 subpopulations: secretory-papillary, secretory-reticular, mesenchymal and pro-inflammatory. Interestingly, the percentage of mesenchymal fibroblast subpopulation is significantly increased in keloid compared to normal scar. Functional studies indicate that mesenchymal fibroblasts are crucial for collagen overexpression in keloid. Increased mesenchymal fibroblast subpopulation is also found in another fibrotic skin disease, scleroderma, suggesting this is a broad mechanism for skin fibrosis. These findings will help us better understand skin fibrotic pathogenesis, and provide potential targets for fibrotic disease therapies.

Date: 2021
References: Add references at CitEc
Citations: View citations in EconPapers (8)

Downloads: (external link)
https://www.nature.com/articles/s41467-021-24110-y Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24110-y

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-021-24110-y

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().