Evidence map›Paper›PMID 33855975›Full record

ArticleThe Journal of clinical investigation2021

The BBSome: a nexus controlling energy metabolism in the brain.

Sandra Blaess, Dagmar Wachten

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 42% 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, 9 citations in OpenAlex.

  1. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Bardet-Biedl Syndrome: Current Perspectives and Clinical Outlook.Therapeutics and clinical risk management · 2023
    Review
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Sandra BlaessNeurodevelopmental Genetics, Institute of Reconstructive Neurobiology and.
Dagmar WachtenInstitute of Innate Immunity, Department of Biophysical Imaging, Medical Faculty, University of Bonn, Bonn, Germany.
NeuroDevelopment Center · USUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bardet-Biedl syndrome (BBS) is a syndromic ciliopathy that has obesity as a cardinal feature. BBS is caused by mutations in BBS genes. BBS proteins control primary cilia function, and BBS mutations therefore lead to dysfunctional primary cilia. Obesity in patients with BBS is mainly caused by hyperphagia due to dysregulated neuronal function in the brain, in particular in the hypothalamus. However, the mechanism by which mutations in BBS genes result in dysfunction in hypothalamic neurons is not well understood. In this issue of the JCI, Wang et al. used BBS and non-BBS patient-derived induced pluripotent stem cells to generate neurons and hypothalamic neurons. Using this human model system, the authors demonstrated that mutations in BBS genes affected primary cilia function, neuronal morphology, and signaling pathways regulating the function of hypothalamic neurons, which control energy homeostasis. This study provides important insights into the mechanisms of BBS-induced obesity.

Indexed as

Bardet-Biedl SyndromeCiliaBrainEnergy MetabolismHumansMicrotubule-Associated ProteinsMicrotubule-Associated Proteins

Identifiers

PMID33855975
PMCPMC8262486
OpenAlexW3156157101

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.