Evidence map›Paper›PMID 35385753›Full record

ArticleCell reports2022

Protein disulfide isomerase modulation of TRPV1 controls heat hyperalgesia in chronic pain.

Yongxue Zhang, Qi Miao, Sai Shi, Han Hao, Xinmeng Li, Zeyao Pu, Yakun Yang, Hailong An, Wei Zhang, Youzhen Kong and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 14 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

16 authors at 4 institutions in 2 countries.

Yongxue ZhangDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China; Department of Pharmacy, The First Hospital of Handan, Handan, Hebei, China.
Qi MiaoDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Sai ShiKey Laboratory of Molecular Biophysics, Institute of Biophysics, School of Science, Hebei University of Technology, Tianjin, Hebei, China.
Han HaoDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Xinmeng LiDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Zeyao PuDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Yakun YangDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Hailong AnKey Laboratory of Molecular Biophysics, Institute of Biophysics, School of Science, Hebei University of Technology, Tianjin, Hebei, China.
Wei ZhangDepartment of Spinal Surgery of the Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Youzhen KongDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Xu PangDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China.
Cunyang GuDepartment of Pathology, The Fourth Hospital of Shijiazhuang, Shijiazhuang, Hebei, China.
Nikita GamperDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China; Faculty of Biological Sciences, University of Leeds, LS2 9JT Leeds, UK.
Yi WuNational Clinical Research Center for Hematologic Diseases, The First Affiliated Hospital, Cyrus Tang Medical Institute, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Prevention, Soochow University, Suzhou 215123, China. Electronic address: wuy@suda.edu.cn.
Hailin ZhangDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China. Electronic address: zhanghl@hebmu.edu.cn.
Xiaona DuDepartment of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China. Electronic address: duxiaona@hebmu.edu.cn.
Hebei Medical University · CNHebei University of Technology · CNHebei University of Engineering · CNSoochow University · CN

Funding

Wellcome Trust 212302Wellcome Trust 212302/Z/18/Z
6 · The paper itself

Abstract

Protein disulfide isomerase (PDI) plays a key role in maintaining cellular homeostasis by mediating protein folding via catalyzing disulfide bond formation, breakage, and rearrangement in the endoplasmic reticulum. Increasing evidence suggests that PDI can be a potential treatment target for several diseases. However, the function of PDI in the peripheral sensory nervous system is unclear. Here we report the expression and secretion of PDI from primary sensory neurons is upregulated in inflammatory and neuropathic pain models. Deletion of PDI in nociceptive DRG neurons results in a reduction in inflammatory and neuropathic heat hyperalgesia. We demonstrate that secreted PDI activates TRPV1 channels through oxidative modification of extracellular cysteines of the channel, indicating that PDI acts as an unconventional positive modulator of TRPV1. These findings suggest that PDI in primary sensory neurons plays an important role in development of heat hyperalgesia and can be a potential therapeutic target for chronic pain.

Indexed as

Chronic PainProtein Disulfide-IsomerasesAnimalsHot TemperatureHumansHyperalgesiaMiceOxidation-ReductionProtein FoldingTRPV Cation ChannelsProtein Disulfide-IsomerasesTRPV1 protein, humanTRPV Cation Channelschronic painCP: Neurosciencecysteine oxidationDRGPDITRPV1

Identifiers

PMID35385753
PMCPMC7618069
OpenAlexW4223577472

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.