Evidence map›Paper›PMID 34938205›Full record

ReviewFrontiers in physiology2021

Ectodysplasin A/Ectodysplasin A Receptor System and Their Roles in Multiple Diseases.

Zhensheng Cai, Xia Deng, Jue Jia, Dong Wang, Guoyue Yuan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Long-Term PMAnnals of the American Thoracic Society · 2025
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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

5 authors at 2 institutions in 1 country.

Zhensheng CaiDepartment of Endocrinology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Xia DengDepartment of Endocrinology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Jue JiaDepartment of Endocrinology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Dong WangDepartment of Endocrinology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Guoyue YuanDepartment of Endocrinology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Affiliated Hospital of Jiangsu University · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ectodysplasin A (EDA) is a member of the tumor necrosis factor (TNF) family of ligands that was initially reported to induce the formation of various ectodermal derivatives during normal prenatal development. EDA exerts its biological activity as two splice variants, namely, EDA-A1 and EDA-A2. The former binds to the EDA receptor (EDAR), resulting in the recruitment of the intracellular EDAR-associated death domain (EDARADD) adapter protein and the activation of the NF-κB signaling pathway, while the latter binds to a different receptor, EDA2R, also known as X-linked ectodermal dysplasia receptor (XEDAR). Inactivation mutation of the EDA gene or the genes coding for its receptors can result in hypohidrosis ectodermal dysplasia (HED), a condition that is characterized by oligotrichosis, edentulosis or oligodontia, and oligohidrosis or anhidrosis. Recently, as a new liver factor, EDA is gradually known and endowed with some new functions. EDA levels were observed to be upregulated in several metabolic diseases, such as non-alcoholic fatty liver disease (NAFLD), obesity, and insulin resistance. In addition, EDA and its receptors have been implicated in tumor pathogenesis through the regulation of tumor cell proliferation, apoptosis, differentiation, and migration. Here, we first review the role of EDA and its two-receptor system in various signaling pathways and then discuss the physiological and pathological roles of EDA and its receptors.

Indexed as

ectodysplasin Aectodysplasin A receptormetabolismsignaling pathwaysskeletal muscle homeostasistumorigenesis

Identifiers

PMID34938205
PMCPMC8685516
OpenAlexW4200344432

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.