Evidence map›Paper›PMID 36901738›Full record

ReviewInternational journal of molecular sciences2023

Histone Deacetylases: Molecular Mechanisms and Therapeutic Implications for Muscular Dystrophies.

Martina Sandonà, Giorgia Cavioli, Alessandra Renzini, Alessia Cedola, Giuseppe Gigli, Dario Coletti, Timothy A McKinsey, Viviana Moresi, Valentina Saccone

Open access · goldFull text readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  19. On RNA-programmable gene modulation as a versatile set of principles targeting muscular dystrophies.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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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

9 authors at 6 institutions in 3 countries.

Martina SandonàIRCCS Fondazione Santa Lucia, 00143 Rome, Italy.
Giorgia CavioliUnit of Histology and Medical Embryology, Department of Human Anatomy, Histology, Forensic Medicine and Orthopedics, University of Rome "La Sapienza", 00161 Rome, Italy.ORCID 0000-0002-1710-4290
Alessandra RenziniUnit of Histology and Medical Embryology, Department of Human Anatomy, Histology, Forensic Medicine and Orthopedics, University of Rome "La Sapienza", 00161 Rome, Italy.ORCID 0000-0002-4265-7188
Alessia CedolaInstitute of Nanotechnology, National Research Council (CNR-NANOTEC), University of Rome "La Sapienza", 00181 Rome, Italy.ORCID 0000-0002-9256-8853
Giuseppe GigliInstitute of Nanotechnology, National Research Council (CNR-NANOTEC), 73100 Lecce, Italy.
Dario ColettiUnit of Histology and Medical Embryology, Department of Human Anatomy, Histology, Forensic Medicine and Orthopedics, University of Rome "La Sapienza", 00161 Rome, Italy.ORCID 0000-0001-7373-1953
Timothy A McKinseyDepartment of Medicine, Division of Cardiology and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Viviana MoresiInstitute of Nanotechnology, National Research Council (CNR-NANOTEC), University of Rome "La Sapienza", 00181 Rome, Italy.ORCID 0000-0003-1912-0339
Valentina SacconeIRCCS Fondazione Santa Lucia, 00143 Rome, Italy.ORCID 0000-0002-0566-6384
Istituto di Nanotecnologia · ITSapienza University of Rome · ITCentre National de la Recherche Scientifique · FRFondazione Santa Lucia · ITUniversità Cattolica del Sacro Cuore · ITUniversity of Colorado Anschutz Medical Campus · US

Funding

Regulation of Chromatin Signaling in Heart Failure by the BRD4 Bromodomain Protein.R01HL127240 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY, SRIVASTAVA, DEEPAK · 2015 to 2022
$6.4M
Deacetylase-Dependent Control of Diastolic Dysfunction and HFpEFR01HL147558 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI HOUSER, STEVEN R, MCKINSEY, TIMOTHY · 2019 to 2022
$3.1M
Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
Small molecule therapies targeting chromatin architecture in heart failureR01HL150225 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MCKINSEY, TIMOTHY, VONDRISKA, THOMAS M. · 2020 to 2023
$2.9M
Screening and Development of Small Molecule HDAC11 Inhibitors to Treat Obesity and Diabetes.R01DK119594 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LIN, HENING, MCKINSEY, TIMOTHY · 2019 to 2022
$2.1M
NHLBI NIH HHS R01 HL116848NHLBI NIH HHS R01 HL127240NHLBI NIH HHS R01 HL147558NHLBI NIH HHS R01 HL150225NIDDK NIH HHS R01 DK119594NIH HHS HL116848, HL147558, DK119594, HL127240, and HL150225
6 · The paper itself

Abstract

Histone deacetylases (HDACs) are enzymes that regulate the deacetylation of numerous histone and non-histone proteins, thereby affecting a wide range of cellular processes. Deregulation of HDAC expression or activity is often associated with several pathologies, suggesting potential for targeting these enzymes for therapeutic purposes. For example, HDAC expression and activity are higher in dystrophic skeletal muscles. General pharmacological blockade of HDACs, by means of pan-HDAC inhibitors (HDACi), ameliorates both muscle histological abnormalities and function in preclinical studies. A phase II clinical trial of the pan-HDACi givinostat revealed partial histological improvement and functional recovery of Duchenne Muscular Dystrophy (DMD) muscles; results of an ongoing phase III clinical trial that is assessing the long-term safety and efficacy of givinostat in DMD patients are pending. Here we review the current knowledge about the HDAC functions in distinct cell types in skeletal muscle, identified by genetic and -omic approaches. We describe the signaling events that are affected by HDACs and contribute to muscular dystrophy pathogenesis by altering muscle regeneration and/or repair processes. Reviewing recent insights into HDAC cellular functions in dystrophic muscles provides new perspectives for the development of more effective therapeutic approaches based on drugs that target these critical enzymes.

Indexed as

Histone DeacetylasesMuscular Dystrophy, DuchenneCarbamatesHistone Deacetylase InhibitorsHumansMuscle, SkeletalCarbamatesgivinostatHistone Deacetylase InhibitorsHistone Deacetylasesclinical trialsDuchenne Muscular Dystrophyhistone deacetylasemuscular dystrophies

Identifiers

PMID36901738
PMCPMC10002075
OpenAlexW4321496918

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read5
identifiers read6
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.