Evidence map›Paper›PMID 35778900›Full record

ReviewSleep2022

Leptin-mediated neural targets in obesity hypoventilation syndrome.

Mateus R Amorim, O Aung, Babak Mokhlesi, Vsevolod Y Polotsky

Open access · greenAbstract readReview
In one paragraph

Review in Sleep, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Sleep and obesity-known interactions and open questions.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2026
    Review
  5. Leptin alleviates obesity hypoventilationbioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Revisiting the Role of Serotonin in Sleep-Disordered Breathing.International journal of molecular sciences · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Mateus R AmorimDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
O AungDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Babak MokhlesiDepartment of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, Rush University Medical Center, Chicago, IL, USA.ORCID 0000-0001-8135-5433
Vsevolod Y PolotskyDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · USRush University Medical Center · US

Funding

Melanocortin 4 signaling in the carotid body in obesityR01HL133100 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Vsevolod Y Polotsky, Wan-yee Tang · 2016 to 2026
$7.1M
Treatment of Sleep Apnea by Targeting Leptin SignalingR01HL128970 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MENDELOWITZ, DAVID, POLOTSKY, VSEVOLOD Y · 2015 to 2023
$5.4M
Intranasal Leptin as A Novel Treatment of Opioid-Induced Respiratory DepressionR61HL156240 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI POLOTSKY, VSEVOLOD Y · 2020 to 2020
$737k
NHLBI NIH HHS R01 HL128970NHLBI NIH HHS R61 HL156240NIH HHS R01 HL128970
6 · The paper itself

Abstract

Obesity hypoventilation syndrome (OHS) is defined as daytime hypercapnia in obese individuals in the absence of other underlying causes. In the United States, OHS is present in 10%-20% of obese patients with obstructive sleep apnea and is linked to hypoventilation during sleep. OHS leads to high cardiorespiratory morbidity and mortality, and there is no effective pharmacotherapy. The depressed hypercapnic ventilatory response plays a key role in OHS. The pathogenesis of OHS has been linked to resistance to an adipocyte-produced hormone, leptin, a major regulator of metabolism and control of breathing. Mechanisms by which leptin modulates the control of breathing are potential targets for novel therapeutic strategies in OHS. Recent advances shed light on the molecular pathways related to the central chemoreceptor function in health and disease. Leptin signaling in the nucleus of the solitary tract, retrotrapezoid nucleus, hypoglossal nucleus, and dorsomedial hypothalamus, and anatomical projections from these nuclei to the respiratory control centers, may contribute to OHS. In this review, we describe current views on leptin-mediated mechanisms that regulate breathing and CO2 homeostasis with a focus on potential therapeutics for the treatment of OHS.

Indexed as

Obesity Hypoventilation SyndromeHumansHypercapniaHypoventilationLeptinObesityLeptinchemoreceptormechanismssleepventilation

Identifiers

PMID35778900
PMCPMC9453616
OpenAlexW4283776353

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.