Evidence map›Paper›PMID 34125373›Full record

ReviewInflammopharmacology2021

Cholinergic anti-inflammatory pathway and connective tissue diseases.

Khalil Hajiasgharzadeh, Alireza Khabbazi, Ahad Mokhtarzadeh, Amir Baghbanzadeh, Zahra Asadzadeh, Elham Adlravan, Behzad Baradaran

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. [Effect of aquaporin 5 on TLR4/MyD88/NF-κB signaling pathway in Sjögren syndrome rats].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
    Article
  4. Article
  5. Review
  6. Observational
  7. Article
  8. Albumin Is a Component of the Esterase Status of Human Blood Plasma.International journal of molecular sciences · 2023
    Article
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

7 authors at 1 institution in 1 country.

Khalil HajiasgharzadehImmunology Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614766, Tabriz, Iran.
Alireza KhabbaziConnective Tissue Diseases Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614756, Tabriz, Iran. dr_khabbazi@yahoo.com.
Ahad MokhtarzadehImmunology Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614766, Tabriz, Iran.
Amir BaghbanzadehImmunology Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614766, Tabriz, Iran.
Zahra AsadzadehImmunology Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614766, Tabriz, Iran.
Elham AdlravanImmunology Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614766, Tabriz, Iran.
Behzad BaradaranImmunology Research Center, Tabriz University of Medical Sciences, Golgasht St, Postcode: 5166614766, Tabriz, Iran. baradaranb@tbzmed.ac.ir.ORCID http://orcid.org/0000-0002-8642-6795
Tabriz University of Medical Sciences · IR

Funding

Tabriz University of Medical Sciences 59256
6 · The paper itself

Abstract

Connective tissue diseases (CTDs) consist of an extensive range of heterogeneous medical conditions, which are caused by immune-mediated chronic inflammation and influences the various connective tissues of the body. They include rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, vasculitis, Sjögren's syndrome, Behcet's disease, and many other autoimmune CTDs. To date, several anti-inflammatory approaches have been developed to reduce the severity of inflammation or its subsequent organ manifestations. As a logical mechanism to harnesses the undesired inflammation, some studies investigated the role of the intrinsic cholinergic anti-inflammatory pathway (CAP) in the modulation of chronic inflammation. Many different experimental and clinical models have been developed to evaluate the therapeutic significance of the CAP in CTDs. On the other hand, an issue that is less emphasized in this regard is the presence of autonomic neuropathy in CTDs, which influences the efficiency of CAP in such clinical settings. This condition occurs during CTDs and is a well-known complication of patients suffering from them. The advantages and limitations of CAP in the control of inflammatory responses and its possible therapeutic benefits in the treatment of CTDs are the main subjects of the current study. Therefore, this narrative review article is provided based on the recent findings of the complicated role of CAP in CTDs which were retrieved by searching Science Direct, PubMed, Google Scholar, and Web of Science. It seems that delineating the complex influences of CAP would be of great interest in designing novel surgical or pharmacological therapeutic strategies for CTDs therapy.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsCholinergic AgentsConnective Tissue DiseasesHumansImplantable NeurostimulatorsInflammation MediatorsNeuroimmunomodulationReceptors, NicotinicSignal Transductionalpha7 Nicotinic Acetylcholine ReceptorCholinergic AgentsInflammation MediatorsReceptors, NicotinicCholinergic anti-inflammatory pathwayConnective tissue diseasesInflammation responseTherapeutic intervention

Identifiers

PMID34125373
OpenAlexW3165975408

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.