Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus

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Standard

Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus. / Christensen, Dan P; Dahllöf, Mattias Salling; Lundh, Morten; Rasmussen, Daniel N; Nielsen, Mette D; Billestrup, Nils; Grunnet, Lars G; Mandrup-Poulsen, Thomas.

I: Molecular Medicine, Bind 17, Nr. 5-6, 2011, s. 378-90.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Christensen, DP, Dahllöf, MS, Lundh, M, Rasmussen, DN, Nielsen, MD, Billestrup, N, Grunnet, LG & Mandrup-Poulsen, T 2011, 'Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus', Molecular Medicine, bind 17, nr. 5-6, s. 378-90. https://doi.org/10.2119/molmed.2011.00021

APA

Christensen, D. P., Dahllöf, M. S., Lundh, M., Rasmussen, D. N., Nielsen, M. D., Billestrup, N., Grunnet, L. G., & Mandrup-Poulsen, T. (2011). Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus. Molecular Medicine, 17(5-6), 378-90. https://doi.org/10.2119/molmed.2011.00021

Vancouver

Christensen DP, Dahllöf MS, Lundh M, Rasmussen DN, Nielsen MD, Billestrup N o.a. Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus. Molecular Medicine. 2011;17(5-6):378-90. https://doi.org/10.2119/molmed.2011.00021

Author

Christensen, Dan P ; Dahllöf, Mattias Salling ; Lundh, Morten ; Rasmussen, Daniel N ; Nielsen, Mette D ; Billestrup, Nils ; Grunnet, Lars G ; Mandrup-Poulsen, Thomas. / Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus. I: Molecular Medicine. 2011 ; Bind 17, Nr. 5-6. s. 378-90.

Bibtex

@article{918185e7d28640df8e3e1a7870e6d5d2,
title = "Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus",
abstract = "Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on interleukin-1{\ss} as a key mediator of insulin resistance and {\ss}-cell failure. In addition to improving insulin resistance and preventing {\ss}-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and HDAC inhibitors (HDACi) promote {\ss}-cell development, proliferation, differentiation and function and positively affect late diabetic microvascular complications. Here we review this evidence and propose that there is a strong rationale for preclinical studies and clinical trials with the aim of testing the utility of HDACi as a novel therapy for diabetes.",
author = "Christensen, {Dan P} and Dahll{\"o}f, {Mattias Salling} and Morten Lundh and Rasmussen, {Daniel N} and Nielsen, {Mette D} and Nils Billestrup and Grunnet, {Lars G} and Thomas Mandrup-Poulsen",
year = "2011",
doi = "10.2119/molmed.2011.00021",
language = "English",
volume = "17",
pages = "378--90",
journal = "Molecular Medicine",
issn = "1076-1551",
publisher = "BioMed Central",
number = "5-6",

}

RIS

TY - JOUR

T1 - Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus

AU - Christensen, Dan P

AU - Dahllöf, Mattias Salling

AU - Lundh, Morten

AU - Rasmussen, Daniel N

AU - Nielsen, Mette D

AU - Billestrup, Nils

AU - Grunnet, Lars G

AU - Mandrup-Poulsen, Thomas

PY - 2011

Y1 - 2011

N2 - Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on interleukin-1ß as a key mediator of insulin resistance and ß-cell failure. In addition to improving insulin resistance and preventing ß-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and HDAC inhibitors (HDACi) promote ß-cell development, proliferation, differentiation and function and positively affect late diabetic microvascular complications. Here we review this evidence and propose that there is a strong rationale for preclinical studies and clinical trials with the aim of testing the utility of HDACi as a novel therapy for diabetes.

AB - Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on interleukin-1ß as a key mediator of insulin resistance and ß-cell failure. In addition to improving insulin resistance and preventing ß-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and HDAC inhibitors (HDACi) promote ß-cell development, proliferation, differentiation and function and positively affect late diabetic microvascular complications. Here we review this evidence and propose that there is a strong rationale for preclinical studies and clinical trials with the aim of testing the utility of HDACi as a novel therapy for diabetes.

U2 - 10.2119/molmed.2011.00021

DO - 10.2119/molmed.2011.00021

M3 - Journal article

C2 - 21274504

VL - 17

SP - 378

EP - 390

JO - Molecular Medicine

JF - Molecular Medicine

SN - 1076-1551

IS - 5-6

ER -

ID: 33901729