1
40
2
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.drudis.2016.10.007" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.drudis.2016.10.007</a>
Pages
352–365
Issue
2
Volume
22
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Emerging strategies of targeting lipoprotein lipase for metabolic and cardiovascular diseases.
Publisher
An entity responsible for making the resource available
Drug Discovery Today
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-02
Subject
The topic of the resource
Animals; Cardiovascular Diseases/drug therapy/*enzymology; Humans; Lipoprotein Lipase/chemistry/*metabolism; Metabolic Diseases/drug therapy/*enzymology
Creator
An entity primarily responsible for making the resource
Geldenhuys Werner J; Lin Li; Darvesh Altaf S; Sadana Prabodh
Description
An account of the resource
Although statins and other pharmacological approaches have improved the management of lipid abnormalities, there exists a need for newer treatment modalities especially for the management of hypertriglyceridemia. Lipoprotein lipase (LPL), by promoting hydrolytic cleavage of the triglyceride core of lipoproteins, is a crucial node in the management of plasma lipid levels. Although LPL expression and activity modulation is observed as a pleiotropic action of some the commonly used lipid lowering drugs, the deliberate development of drugs targeting LPL has not occurred yet. In this review, we present the biology of LPL, highlight the LPL modulation property of currently used drugs and review the novel emerging approaches to target LPL.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.drudis.2016.10.007" target="_blank" rel="noreferrer noopener">10.1016/j.drudis.2016.10.007</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Animals
Cardiovascular Diseases/drug therapy/*enzymology
Darvesh Altaf S
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Drug Discovery Today
Geldenhuys Werner J
Humans
Lin Li
Lipoprotein Lipase/chemistry/*metabolism
Metabolic Diseases/drug therapy/*enzymology
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Sadana Prabodh
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.drudis.2014.05.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.drudis.2014.05.001</a>
Pages
1601–1606
Issue
10
Volume
19
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
mitoNEET as a novel drug target for mitochondrial dysfunction.
Publisher
An entity responsible for making the resource available
Drug Discovery Today
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-10
Subject
The topic of the resource
Animals; Drug Delivery Systems; Energy Metabolism; Humans; Mitochondria/*metabolism; Mitochondrial Proteins/chemistry/*metabolism; Protein Conformation; Thiazolidinediones/pharmacology
Creator
An entity primarily responsible for making the resource
Geldenhuys Werner J; Leeper Thomas C; Carroll Richard T
Description
An account of the resource
Mitochondrial dysfunction plays an important part in the pathology of several diseases, including Alzheimer's disease and Parkinson's disease. Targeting mitochondrial proteins shows promise in treating and attenuating the neurodegeneration seen in these diseases, especially considering their complex and pleiotropic origins. Recently, the mitochondrial protein mitoNEET [also referred to as CDGSH iron sulfur domain 1 (CISD1)] has emerged as the mitochondrial target of thiazolidinedione drugs such as the antidiabetic pioglitazone. In this review, we evaluate the current understanding regarding how mitoNEET regulates cellular bioenergetics as well as the structural requirements for drug compound association with mitoNEET. With a clear understanding of mitoNEET function, it might be possible to develop therapeutic agents useful in several different diseases including neurodegeneration, breast cancer, diabetes and inflammation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.drudis.2014.05.001" target="_blank" rel="noreferrer noopener">10.1016/j.drudis.2014.05.001</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Animals
Carroll Richard T
Drug Delivery Systems
Drug Discovery Today
Energy Metabolism
Geldenhuys Werner J
Humans
Leeper Thomas C
Mitochondria/*metabolism
Mitochondrial Proteins/chemistry/*metabolism
Protein Conformation
Thiazolidinediones/pharmacology