Evidence map›Paper›PMID 42034790›Full record

ArticleCell death and differentiation2026

Endothelial USP2a-METTL16 loop potentiates IL-6 signaling via m

Hanqing Zhu, Ping Yuan, Xiangyang Wu, Yuxia Huang, Wentian Zhang, Xingxing Sun, Jianhua Xu, Tianran Zhou, Junfang Xu, Li Chen and 5 more

Abstract read
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In one paragraph

Article in Cell death and differentiation, 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
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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

15 authors.

Hanqing Zhu *Department of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID http://orcid.org/0000-0002-3104-1302
Ping Yuan *Department of Cardio-Pulmonary Circulation, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Xiangyang WuInnovation and Incubation Center, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID http://orcid.org/0000-0002-0444-7120
Yuxia HuangDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Institute of Respiratory Diseases of Sun Yat-sen University, Guangzhou, China.
Wentian ZhangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID http://orcid.org/0000-0003-3332-0476
Xingxing SunDepartment of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Jianhua XuDepartment of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Tianran ZhouDepartment of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Junfang XuClinical and Translational Research Center, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Li ChenInnovation and Incubation Center, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Wenlan YangDepartment of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Jinming LiuDepartment of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China.
Haipeng LiuClinical and Translational Research Center, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China. haipengliu@tongji.edu.cn.ORCID http://orcid.org/0000-0002-3338-6291
Fenghou GaoDepartment of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. fenghougao@163.com.
Jian GuoDepartment of Pulmonary Function Test, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, China. jianjian11121978@163.com.ORCID http://orcid.org/0009-0000-8384-7968

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82103309National Natural Science Foundation of China (National Science Foundation of China) 82201931National Natural Science Foundation of China (National Science Foundation of China) 82370057National Natural Science Foundation of China (National Science Foundation of China) 82400061Natural Science Foundation of Shanghai (Natural Science Foundation of Shanghai Municipality) 24ZR1460100
6 · The paper itself

Abstract

Dysfunction of vascular endothelial cells is recognized as a critical driver in pulmonary vascular remodeling of pulmonary hypertension (PH). Although interleukin-6 (IL-6) has been firmly established as an indispensable factor leading to pulmonary vascular remodeling, its downstream molecular mechanisms remain incompletely elucidated. Here, we discover that ubiquitin-specific protease 2a (USP2a) is upregulated in lung tissues of PH patients and preclinical PH models, and in IL-6-stimulated endothelial cells. Both the endothelial cell-specific Usp2a genetic deletion and the pharmacological inhibition of USP2a with the inhibitor ML364 alleviate experimental PH manifestations. Mechanistically, USP2a attenuates the degradation of methyltransferase-like 16 (METTL16) by deubiquitination. Notably, METTL16 reciprocally enhances USP2a expression via interactions with eIF3a and eIF3b in a methyltransferase activity-independent manner, establishing a self-reinforcing USP2a-METTL16 regulatory loop. Subsequent investigations reveal that METTL16 enhances N6-methyladenosine (m

Identifiers

PMID42034790

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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.