Education
Shanghai Jiao Tong University Shanghai, China
Master of Science (MSc) in Medicine (Plastic and Reconstructive Surgery) 2022 – Present
- Research topic: RNA modificationof skin regeneration
Huazhong University of Science and Technology Wuhan, China
Bachelor of Medicine, Bachelor of Surgery (MBBS) 2017 – 2022
- Honours Degree• Overall GPA:3.99/4.0 Rank: 3rd/126
Sidney Sussex College, University of Cambridge Cambridge, England
Cambridge Academic Development Programme Aug. 2019
Publications
[1] ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis.
Xu R#, Yang E#, Liang H, Luo S, Liu Y, Khoong Y, Li H, Huang X#, *, Zhao Y*, Zan T*.
Clinical and Translational Medicine. 2024 Sep;14(9): e70016.
[2] ALKBH3-mediated m1A demethylation of METTL3 endows pathological fibrosis: Interplay between m1A and m6A RNA methylation.
Tu L#, Gu S#, Xu R#, Yang E#, Huang X, Liang H, Luo S, Li H*, Zhao Y*, Zan T*.
Advanced Science. 2025 Feb 28:e2417067.
[3] Single cell deciphering of pruritic keloids: the interaction between fibroblasts and Schwann cells through the Midkine signaling.
Yang E#, Xu R#, Tu L#, Zhang H, Luo S, Liang H, Liu Y, Gu S, Zhao Y, Huang X*, Zan T*. Burns & Trauma. 2025 Apr.
[4] Deciphering pain and pruritus in keloid from the perspective of Neuropathy: where are we now?
Yang E#, Xu R#, Huang X*, Zan T*.
Biomedicines. 2025, 13,663.
[5] Targeting the nuclear long noncoding transcript LSP1P5 abrogates extracellular matrix deposition by trans-upregulating CEBPA in keloids.
Gu S#, Huang X#, Luo S#, Liu Y, Khoong Y, Liang H, Tu L, Xu R, Yang E, Zhao Y*, Yao M*, Zan T*.
Molecular Therapy. 2024 Jun 5;32(6):1984-1999.
[6] Interleukin 11 drives dermal fibroblast activation in mechanical stretch-mediated skin expansion.
Liu Y#, Khoong Y#, Xia W#, Xu R, Anissa W, Liang H, Luo S, Yang E, Huang X*, Zan T*.
Journal of Investigative Dermatology. 2024 Apr.
[7] A treatment recommendation for trichoepithelioma: Thoughts on selection of treatment timing and method.
Luo S, Gu S, Xu R, Yang E, Tu L, Liang H, Huang X, Ren J*, Zan T*.
Chinese Journal of Plastic and Reconstructive Surgery. 2024,6(1):37-40
[8] Re: “The Detroit Keloid Scale: A Validated Tool for Rating Keloids” by Lyons et al.
Xu R#, Huang X#, Zan T*.
Facial Plastic Surgery & Aesthetic Medicine. 2024 Nov-Dec;26(6):782-783.
[9] Whole exome sequencing identifies three novel gene mutations in patients with the triad of diabetic ketoacidosis, hypertriglyceridemia, and acute pancreatitis.
Huang Z#, Xu Z#, Xu R#, Huang L, Xu X, Lai X*.
Journal of Diabetes. 2021 Mar;13(3):200-210.
[10] The relationship between Long Noncoding RNA (lncRNA) Small Nucleolar RNA Host Gene 12 (SNHG12) expression in solid malignant tumors and prognosis of tumor patients: A systematic review and meta-analysis.
Huang Z#, Zhuo W#, Xu R, Wu Z, Xiong Y, Xu Z*.
Medicine (Baltimore). 2020 Oct 9;99(41): e22247.
Abstract submitted for the 5th International Keloid Symposium
Title: ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis
AUTHORS: Ruoqing Xu1, En Yang1, Hsin Liang1, Shenying Luo1, Yunhan Liu1, Yimin Khoong1, Haizhou Li1, Xin Huang1, Yixuan Zhao1, Tao Zan1.
AUTHORS’ AFFILIATIONS:
Department of Plastic and Reconstructive Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China
Background: Elevated extracellular matrix (ECM) accumulation is a major contributing factor to the pathogenesis of fibrotic diseases. Recent studies have indicated that N6-methyladenosine (m6A) RNA modification plays a pivotal role in modulating RNA stability and contribute to the initiation of various pathological conditions. Howbeit, the precise mechanism by which m6A influences ECM deposition remains unclear.
Methods: In this study, we used hypertrophic scars (HTSs) as a paradigm to
investigate ECM-related diseases. We focused on the role of ALKBH5-mediated m6A demethylation within the pathological progression of HTSs and examined its correlation with clinical stages. The effects of ALKBH5 ablation on ECM components were studied both in vivo and in vitro. Downstream targets of ALKBH5, along with their underlying mechanisms, were identified using integrated high-throughput analysis, RNA-binding protein immunoprecipitation and RNA pull-down assays. Furthermore, the therapeutic potential of exogenous ALKBH5 overexpression was evaluated in fibrotic scar models.
Results:
ALKBH5 was decreased in fibroblasts derived from HTS lesions and was negatively correlated with their clinical stages. Importantly, ablation of ALKBH5 promoted the expression of COL3A1, COL1A1, and ELN, leading to pathological deposition and reconstruction of the ECM both in vivo and in vitro. From a therapeutic perspective, the exogenous overexpression of ALKBH5 significantly inhibited abnormal collagen deposition in fibrotic scar models. As determined by integrated high-throughput analysis, key ECM components includingCOL3A1, COL1A1, and ELN are direct downstream targets of ALKBH5. By means of its mechanism, ALKBH5 inhibits the expression of COL3A1, COL1A1, and ELN by removing m6A from mRNAs, thereby decreasing their stability in a YTHDF1-dependent manner.
Conclusion:
Our study identified ALKBH5 as an endogenous suppressor of pathological ECM deposition, contributing to the development of a reprogrammed m6A-targeted therapy for HTSs.
