Evidence map›Paper›PMID 27388987›Full record

ReviewNature reviews. Endocrinology2016

The pathophysiology of defective proteostasis in the hypothalamus - from obesity to ageing.

Cláudia Cavadas, Célia A Aveleira, Gabriela F P Souza, Lício A Velloso

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
14.1field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  3. Review
  4. The Long Non-coding RNA Landscape of Endurance Exercise Training.bioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Article
  7. Proteostasis signatures in human diseases.PLoS computational biology · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Microglia in Central Control of Metabolism.Physiology (Bethesda, Md.) · 2024
    Review
  12. DNA Methylation in the Hypothalamic Feeding Center and Obesity.Journal of obesity & metabolic syndrome · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Arcuate Nucleus Overexpression of NHLH2 Reduces Body Mass and Attenuates Obesity-Associated Anxiety/Depression-like Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  19. Nutritional factors regulating behavior and biological clocks.Archives of endocrinology and metabolism · 2021
    Article
  20. 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

4 authors at 2 institutions in 2 countries.

Cláudia CavadasCenter for Neuroscience and Cell Biology, University of Coimbra, Coimbra, 3004-504, Portugal.
Célia A AveleiraCenter for Neuroscience and Cell Biology, University of Coimbra, Coimbra, 3004-504, Portugal.
Gabriela F P SouzaLaboratory of Cell Signaling, Obesity and Comorbidities Research Center, University of Campinas, Campinas, 1308-970, Brazil.
Lício A VellosoLaboratory of Cell Signaling, Obesity and Comorbidities Research Center, University of Campinas, Campinas, 1308-970, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BRUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothalamic dysfunction has emerged as an important mechanism involved in the development of obesity and its comorbidities, as well as in the process of ageing and age-related diseases, such as type 2 diabetes mellitus, hypertension and Alzheimer disease. In both obesity and ageing, inflammatory signalling is thought to coordinate many of the cellular events that lead to hypothalamic neuronal dysfunction. This process is triggered by the activation of signalling via the toll-like receptor 4 pathway and endoplasmic reticulum stress, which in turn results in intracellular inflammatory signalling. However, the process that connects inflammation with neuronal dysfunction is complex and includes several regulatory mechanisms that ultimately control the homeostasis of intracellular proteins and organelles (also known as 'proteostasis'). This Review discusses the evidence for the key role of proteostasis in the control of hypothalamic neurons and the involvement of this process in regulating whole-body energy homeostasis and lifespan.

Indexed as

AgingAlzheimer DiseaseDiabetes Mellitus, Type 2Endoplasmic Reticulum StressHomeostasisHumansHypertensionHypothalamusInflammationNeuronsObesityOrganellesProteinsProteostasis DeficienciesSignal TransductionToll-Like Receptor 4ProteinsToll-Like Receptor 4

Identifiers

PMID27388987
OpenAlexW2467492332

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.