Evidence map›Paper›PMID 29958910›Full record

ArticleEBioMedicine2018

Programming and Regulation of Metabolic Homeostasis by HDAC11.

Lei Sun, Caralina Marin de Evsikova, Ka Bian, Alexandra Achille, Elphine Telles, Huadong Pei, Edward Seto

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

74 citing papers in PubMed, 121 citations in OpenAlex.

  1. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
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  19. Targeting Histone Deacetylase 11 with a Highly Selective Inhibitor for the Treatment of MASLD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Lei SunGeorge Washington University Cancer Center, USA; Department of Biochemistry & Molecular Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC 20037, USA.
Caralina Marin de EvsikovaDepartment of Molecular Medicine, Morsani College of Medicine, USA.
Ka BianGeorge Washington University Cancer Center, USA; Department of Biochemistry & Molecular Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC 20037, USA.
Alexandra AchilleMoffitt Cancer Center, University of South Florida, Tampa, FL 33612, USA.
Elphine TellesGeorge Washington University Cancer Center, USA.
Huadong PeiGeorge Washington University Cancer Center, USA; Department of Biochemistry & Molecular Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC 20037, USA.
Edward SetoGeorge Washington University Cancer Center, USA; Department of Biochemistry & Molecular Medicine, George Washington University School of Medicine & Health Sciences, Washington, DC 20037, USA. Electronic address: seto@gwu.edu.
George Washington University · USUniversity of South Florida · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI Christine O'Connell · 1998 to 2026
$93.5M
NCI NIH HHS P30 CA076292
6 · The paper itself

Abstract

Histone deacetylases (HDACs) are enzymes that regulate protein functions by catalyzing the removal of acetyl and acyl groups from lysine residues. They play pivotal roles in governing cell behaviors and are indispensable in numerous biological processes. HDAC11, the last identified and sole member of class IV HDACs, was reported over a decade ago. However, its physiological function remains poorly understood. Here, we report that HDAC11 knockout mice are resistant to high-fat diet-induced obesity and metabolic syndrome, suggesting that HDAC11 functions as a crucial metabolic regulator. Depletion of HDAC11 significantly enhanced insulin sensitivity and glucose tolerance, attenuated hypercholesterolemia, and decreased hepatosteatosis and liver damage. Mechanistically, HDAC11 deficiency boosts energy expenditure through promoting thermogenic capacity, which attributes to the elevation of uncoupling protein 1 (UCP1) expression and activity in brown adipose tissue. Moreover, loss of HDAC11 activates the adiponectin-AdipoR-AMPK pathway in the liver, which may contribute to a reversal in hepatosteatosis. Overall, our findings distinguish HDAC11 as a novel regulator of obesity, with potentially important implications for obesity-related disease treatment.

Indexed as

AnimalsDiet, High-FatDisease Models, AnimalEnergy MetabolismFatty LiverGene Knockout TechniquesGlucose Tolerance TestHistone DeacetylasesHomeostasisInsulin ResistanceLiverMetabolic SyndromeMiceObesitySignal TransductionThermogenesisHdac11 protein, mouseHistone DeacetylasesUcp1 protein, mouseUncoupling Protein 1AdiponectinCPT1HDAC11Hepatic steatosisMetabolic syndromeObesityUCP1

Identifiers

PMID29958910
PMCPMC6085537
OpenAlexW2810056186

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.