Evidence map›Paper›PMID 38862980›Full record

ReviewClinical epigenetics2024

Exploring histone deacetylases in type 2 diabetes mellitus: pathophysiological insights and therapeutic avenues.

Kukkala Kiran Kumar, Elhadi Husein Aburawi, Milos Ljubisavljevic, Melvin Khee Shing Leow, Xu Feng, Suraiya Anjum Ansari, Bright Starling Emerald

Abstract readReview
In one paragraph

Review in Clinical epigenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. 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

7 authors.

Kukkala Kiran KumarDepartment of Anatomy, College of Medicine and Health Sciences, United Arab Emirates University, PO Box 15551, Al Ain, Abu Dhabi, United Arab Emirates.
Elhadi Husein AburawiDepartment of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates.
Milos LjubisavljevicDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates.
Melvin Khee Shing LeowLKC School of Medicine, Nanyang Technological University, Singapore, Singapore.
Xu FengDepartment of Biochemistry, YLL School of Medicine, National University of Singapore, Singapore, Singapore.
Suraiya Anjum AnsariDepartment of Biochemistry, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi, United Arab Emirates.
Bright Starling EmeraldDepartment of Anatomy, College of Medicine and Health Sciences, United Arab Emirates University, PO Box 15551, Al Ain, Abu Dhabi, United Arab Emirates. bsemerald@uaeu.ac.ae.

Funding

ASPIRE, the technology program management pillar of Abu Dhabi's Advanced Technology Research Council (ATRC) ASPIRE Precision Medicine Research Institute Abu Dhabi (VRI-20-10)College of Medicine and Health Sciences, United Arab Emirates University Faculty grant 3IM279, 12M086United Arab Emirates University UAEU-IIT collaborative grant 31M492/12M053Zayed Bin Sultan Charitable and Humanitarian Foundation (ZCHF) Grant 21R110
6 · The paper itself

Abstract

Diabetes mellitus is a chronic disease that impairs metabolism, and its prevalence has reached an epidemic proportion globally. Most people affected are with type 2 diabetes mellitus (T2DM), which is caused by a decline in the numbers or functioning of pancreatic endocrine islet cells, specifically the β-cells that release insulin in sufficient quantity to overcome any insulin resistance of the metabolic tissues. Genetic and epigenetic factors have been implicated as the main contributors to the T2DM. Epigenetic modifiers, histone deacetylases (HDACs), are enzymes that remove acetyl groups from histones and play an important role in a variety of molecular processes, including pancreatic cell destiny, insulin release, insulin production, insulin signalling, and glucose metabolism. HDACs also govern other regulatory processes related to diabetes, such as oxidative stress, inflammation, apoptosis, and fibrosis, revealed by network and functional analysis. This review explains the current understanding of the function of HDACs in diabetic pathophysiology, the inhibitory role of various HDAC inhibitors (HDACi), and their functional importance as biomarkers and possible therapeutic targets for T2DM. While their role in T2DM is still emerging, a better understanding of the role of HDACi may be relevant in improving insulin sensitivity, protecting β-cells and reducing T2DM-associated complications, among others.

Indexed as

Diabetes Mellitus, Type 2Epigenesis, GeneticHistone Deacetylase InhibitorsHistone DeacetylasesAnimalsHumansInsulinInsulin ResistanceInsulin-Secreting CellsOxidative StressHistone Deacetylase InhibitorsHistone DeacetylasesInsulinDiabetes mellitusFunctional analysisHDAC inhibitorsHDACsInsulinPancreatic β-cells

Identifiers

PMID38862980
PMCPMC11167878

What OpenQuestion holds

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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.