Evidence map›Paper›PMID 37175930›Full record

ReviewInternational journal of molecular sciences2023

Rahul Pandey, Marina Bakay, Hakon Hakonarson

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Eosinophilic gastrointestinal diseases.Nature reviews. Disease primers · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025
    Review
  9. Review
  10. AnFrontiers in genetics · 2025
    Article
  11. Defining Mechanistic Links Between the Non-Coding Variant rs17673553 inInternational journal of molecular sciences · 2025
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Autophagy Dysfunction: The Kernel of Hair Loss?Clinical, cosmetic and investigational dermatology · 2024
    Review
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Rahul PandeyCenter for Applied Genomics, Children's Hospital of Philadelphia, Abramson Research Center, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318, USA.
Marina BakayCenter for Applied Genomics, Children's Hospital of Philadelphia, Abramson Research Center, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318, USA.
Hakon HakonarsonCenter for Applied Genomics, Children's Hospital of Philadelphia, Abramson Research Center, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318, USA.
Children's Hospital of Philadelphia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CLEC16A is emerging as an important genetic risk factor for several autoimmune disorders and for Parkinson disease (PD), opening new avenues for translational research and therapeutic development. While the exact role of CLEC16A in health and disease is still being elucidated, the gene plays a critical role in the regulation of autophagy, mitophagy, endocytosis, intracellular trafficking, immune function, and in biological processes such as insulin secretion and others that are important to cellular homeostasis. As shown in both human and animal modeling studies, CLEC16A hypofunction predisposes to both autoinflammatory phenotype and neurodegeneration. While the two are clearly related, further functional studies are needed to fully understand the mechanisms involved for optimized therapeutic interventions. Based on recent data, mitophagy-inducing drugs may be warranted, and such therapy should be tested in clinical trials as these drugs would tackle the underlying pathogenic mechanism (s) and could treat or prevent symptoms of autoimmunity and neurodegeneration in individuals with

Indexed as

Autoimmune DiseasesLectins, C-TypeAnimalsAutoimmunityAutophagyHumansMonosaccharide Transport ProteinsRisk FactorsCLEC16A protein, humanLectins, C-TypeMonosaccharide Transport ProteinsautoimmunityautophagyCLEC16AC-type lectin-like domain family 16A (CLEC16A) genegenome-wide association studies (GWAS)mitophagyneurodegenerationParkinson’s disease (PD)suppressor of cytokine signaling 1 (SOCS1)susceptibility locitype 1 diabetes (T1D)

Identifiers

PMID37175930
PMCPMC10179542
OpenAlexW4376599825

What OpenQuestion 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 OpenQuestion graph.