Mechanisms of heart failure with preserved ejection fraction in the presence of diabetes mellitus

Lazar, S; Rayner, B; Lopez Campos, G; McGrath, K; McClements, L

Mechanisms of heart failure with preserved ejection fraction in the presence of diabetes mellitus

Lazar, S Rayner, B Lopez Campos, G McGrath, K

McClements, L

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Publisher:: Elsevier BV
Publication Type:: Journal Article
Citation:: Translational Metabolic Syndrome Research, 2020, 3, pp. 1-5
Issue Date:: 2020-04-08

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Field	Value	Language
dc.contributor.author	Lazar, S
dc.contributor.author	Rayner, B
dc.contributor.author	Lopez Campos, G
dc.contributor.author	McGrath, K https://orcid.org/0000-0002-6244-3929
dc.contributor.author	McClements, L https://orcid.org/0000-0002-4911-1014
dc.date.accessioned	2020-12-18T02:29:32Z
dc.date.available	2020-12-18T02:29:32Z
dc.date.issued	2020-04-08
dc.identifier.citation	Translational Metabolic Syndrome Research, 2020, 3, pp. 1-5
dc.identifier.issn	2588-9303
dc.identifier.issn	2588-9303
dc.identifier.uri	http://hdl.handle.net/10453/144834
dc.description.abstract	Cardiovascular disease (CVD) is the leading cause of death globally. People living with type 2 diabetes mellitus (T2DM) have a three times higher risk of developing CVD, particularly heart failure with preserved ejection fraction (HFpEF), for which there is no treatment. The need for tangible interventions has led to investigations into a number of biomarkers associated with metabolic and vascular dysfunction that could be utilised for diagnostic and treatment purposes. This review discusses the importance and mechanisms of inflammatory and angiogenic biomarkers, which have shown the most potential in the pathogenesis and diagnosis of HFpEF in the presence of diabetes. In depth “in silico” analysis was also carried out to identify pathogenic pathways associated with HFpEF, both in the presence and absence of diabetes. The results identified mostly inflammatory pathways associated with HFpEF in the presence of diabetes, and a number of pathways related to angiogenesis, remodelling and metabolism. In addition, the results also identified inflammation, in the absence of diabetes. The shared and unique pathways identified in HFpEF in the presence and absence of diabetes, should be explored further in order to improve management and outcomes of people living with HFpEF.
dc.language	en
dc.publisher	Elsevier BV
dc.relation.ispartof	Translational Metabolic Syndrome Research
dc.relation.isbasedon	10.1016/j.tmsr.2020.04.002
dc.rights	info:eu-repo/semantics/openAccess
dc.title	Mechanisms of heart failure with preserved ejection fraction in the presence of diabetes mellitus
dc.type	Journal Article
utslib.citation.volume	3
utslib.location.activity	Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - IBMD - Initiative for Biomedical Devices
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	open_access	*
pubs.consider-herdc	false
dc.date.updated	2020-12-18T02:29:19Z
pubs.publication-status	Published online
pubs.volume	3

Abstract:

Cardiovascular disease (CVD) is the leading cause of death globally. People living with type 2 diabetes mellitus (T2DM) have a three times higher risk of developing CVD, particularly heart failure with preserved ejection fraction (HFpEF), for which there is no treatment. The need for tangible interventions has led to investigations into a number of biomarkers associated with metabolic and vascular dysfunction that could be utilised for diagnostic and treatment purposes. This review discusses the importance and mechanisms of inflammatory and angiogenic biomarkers, which have shown the most potential in the pathogenesis and diagnosis of HFpEF in the presence of diabetes. In depth “in silico” analysis was also carried out to identify pathogenic pathways associated with HFpEF, both in the presence and absence of diabetes. The results identified mostly inflammatory pathways associated with HFpEF in the presence of diabetes, and a number of pathways related to angiogenesis, remodelling and metabolism. In addition, the results also identified inflammation, in the absence of diabetes. The shared and unique pathways identified in HFpEF in the presence and absence of diabetes, should be explored further in order to improve management and outcomes of people living with HFpEF.

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http://hdl.handle.net/10453/144834