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Cardiovascular Complications of Diabetes
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Cardiovascular Complications of Diabetes

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 18282

Special Issue Editors

Prof. Dr. Peter J. Little

E-Mail Website
Guest Editor
1. School of Pharmacy, Pharmacy Australia Centre of Excellence, The University of Queensland, Woolloongabba 4102, Queensland, Australia
2. Deperatnment of Pharmacy, Xinhua College of Sun Yat sen University, Tianhe District, Guangzhou 510520, Guangdong, China
Interests: diabetes; cardiovascular complications; atherosclerosis; proteoglycans and glycosaminoglycans; cellular signaling; Smad transcription factors; natural product pharmacology
Special Issues, Collections and Topics in MDPI journals
Dr. Danielle Kamato

E-Mail Website
Guest Editor
School of Pharmacy, Pharmacy Australia Centre of Excellence, The University of Queensland, Woolloongabba, QLD 4102, Australia
Interests: atherosclerosis; endothelial dysfunction; Smad transcription factor; proteoglycans, G protein coupled receptors; cell signalling

Special Issue Information

Dear Colleagues,

There are three main elements to diabetes mellitus—the immunology of Type 1 diabetes, the dysmetabolic state of Type 2 diabetes, and the cardiovascular complications of diabetes. The vascular diseases of diabetes are known as microvascular and macrovascular disease. Microvascular disease occurs as retinopathy, neuropathy, and nephropathy, and macrovascular disease as atherosclerosis underlying strokes and heart attacks. There is very strong evidence that hyperglycaemia drives microvascular disease and attenuating hyperglycaemia prevents microvascular disease. However, the role of hyperglycaemia in driving macrovascular disease has been controversial. There is also a therapeutic dilemma—it does not follow automatically that if a risk factor causes disease, treating the risk factor reverses or prevents the disease, possibly because of a mismatch between the mechanism causing and mode of action of the pharmacological agent in reversing the risk factor, in this case hyperglycaemia. Insulin resistance also plays a major role in Type 2 and possibly Type 1 diabetes, and discerning the biochemical mechanism of insulin resistance has proven to be a very difficult undertaking. Whereas early agents did not prevent cardiovascular deaths from diabetes, the landscape has changed dramatically in recent years where several new classes of agents, notably sodium–glucose co-transporter 2 inhibitors (SGLT2i), can prevent diabetes-associated events and deaths in clinical trials and the community. Most recently, there has been an emerging body of work related to the actions of natural products in preventing hyperglycaemia in an array of animal models; most of these are speculated to be due to anti-oxidative mechanisms, but no real targets have emerged that can be taken further to a new therapeutic agent for clinical use.

In this context, we seek experimental papers at the cellular, animal model or clinical level and insightful reviews, which:

  • Define the mechanisms through which hyperglycaemia and insulin resistance cause cardiovascular diseases;
  • Examine mechanisms and pathways for preventing hyperglycaemia and cardiovascular disease;
  • Provide new insights into the role of natural products in protecting against the cardiovascular complications of diabetes;
  • Define the efficacy of new and emerging anti-hyperglycaemic medicines in preventing diabetes-associated cardiovascular disease.

Prof. Dr. Peter J. Little
Dr. Danielle Kamato
Guest Editors

Manuscript Submission Information

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Keywords

  • cardiovascular disease
  • diabetes mellitus
  • atherosclerosis
  • inflammation
  • oxidative stress
  • fibrosis
  • thrombosis
  • endothelial dysfunction
  • medical therapy of hyperglycaemia

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Published Papers (4 papers)

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Research

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21 pages, 3814 KiB  
Article
The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice
by Sarah A Marshall, Cheng Xue Qin, Maria Jelinic, Kelly O’Sullivan, Minh Deo, Jesse Walsh, Mandy Li, Laura J Parry, Rebecca H. Ritchie and Chen Huei Leo
Int. J. Mol. Sci. 2020, 21(4), 1384; https://doi.org/10.3390/ijms21041384 - 18 Feb 2020
Cited by 28 | Viewed by 4125
Abstract
The formyl peptide receptor (FPR) family are a group of G-protein coupled receptors that play an important role in the regulation of inflammatory processes. It is well-established that activation of FPRs can have cardioprotective properties. Recently, more stable small-molecule FPR1/2 agonists have been [...] Read more.
The formyl peptide receptor (FPR) family are a group of G-protein coupled receptors that play an important role in the regulation of inflammatory processes. It is well-established that activation of FPRs can have cardioprotective properties. Recently, more stable small-molecule FPR1/2 agonists have been described, including both Compound 17b (Cmpd17b) and Compound 43 (Cmpd43). Both agonists activate a range of signals downstream of FPR1/2 activation in human-engineered FPR-expressing cells, including ERK1/2 and Akt. Importantly, Cmpd17b (but not Cmpd43) favours bias away from intracellular Ca2+ mobilisation in this context, which has been associated with greater cardioprotection in response to Cmpd17b over Cmpd43. However, it is unknown whether these FPR agonists impact vascular physiology and/or elicit vasoprotective effects in the context of diabetes. First, we localized FPR1 and FPR2 receptors predominantly in vascular smooth muscle cells in the aortae of male C57BL/6 mice. We then analysed the vascular effects of Cmpd17b and Cmpd43 on the aorta using wire-myography. Cmpd17b but not Cmpd43 evoked a concentration-dependent relaxation of the mouse aorta. Removal of the endothelium or blockade of endothelium-derived relaxing factors using pharmacological inhibitors had no effect on Cmpd17b-evoked relaxation, demonstrating that its direct vasodilator actions were endothelium-independent. In aortae primed with elevated K+ concentration, increasing concentrations of CaCl2 evoked concentration-dependent contraction that is abolished by Cmpd17b, suggesting the involvement of the inhibition of Ca2+ mobilisation via voltage-gated calcium channels. Treatment with Cmpd17b for eight weeks reversed endothelial dysfunction in STZ-induced diabetic aorta through the upregulation of vasodilator prostanoids. Our data indicate that Cmpd17b is a direct endothelium-independent vasodilator, and a vasoprotective molecule in the context of diabetes. Full article
(This article belongs to the Special Issue Cardiovascular Complications of Diabetes)
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14 pages, 5448 KiB  
Article
Hydrogen Sulfide Prevents Elastin Loss and Attenuates Calcification Induced by High Glucose in Smooth Muscle Cells through Suppression of Stat3/Cathepsin S Signaling Pathway
by Ye-Bo Zhou, Hong Zhou, Li Li, Ying Kang, Xu Cao, Zhi-Yuan Wu, Lei Ding, Gautam Sethi and Jin-Song Bian
Int. J. Mol. Sci. 2019, 20(17), 4202; https://doi.org/10.3390/ijms20174202 - 27 Aug 2019
Cited by 42 | Viewed by 3955
Abstract
Vascular calcification can be enhanced by hyperglycemia. Elastin loss in tunica media promotes the osteogenic transformation of smooth muscle cells (SMCs) and involves arterial medial calcification (AMC) that is associated with a high incidence of cardiovascular risk in patients with type 2 diabetes. [...] Read more.
Vascular calcification can be enhanced by hyperglycemia. Elastin loss in tunica media promotes the osteogenic transformation of smooth muscle cells (SMCs) and involves arterial medial calcification (AMC) that is associated with a high incidence of cardiovascular risk in patients with type 2 diabetes. Here, we tested whether hydrogen sulfide (H2S), an endogenous gaseous mediator, can prevent elastin loss and attenuate calcification induced by high glucose in SMCs. Calcification was induced by high glucose (4500 mg/L) in human aortic SMCs (HASMCs) under the condition of calcifying medium containing 10 mM β-glycerophosphate (β-GP). The experiments showed that NaHS (an H2S donor, 100 μM) mitigated the calcification of HASMCs treated with high glucose by decreasing calcium and phosphorus levels, calcium deposition and ALP activity and inhibited osteogenic transformation by increasing SMα-actin and SM22α, two phenotypic markers of smooth muscle cells, and decreasing core binding factor α-1 (Cbfα-1), a key factor in bone formation, protein expressions in HASMCs. Moreover, NaHS administration inhibited the activation of Stat3, cathepsin S (CAS) activity and its expression, but increased the level of elastin protein. Pharmacological inhibition or gene silencing Stat3 not only reversed elastin loss, but also attenuated CAS expression. Inhibition of CAS alleviated, while CAS overexpression exacerbated, elastin loss. Interestingly, overexpression of wild type (WT)-Stat3, but not its mutant C259S, elevated CAS protein expression and reduced elastin level. Moreover, NaHS induced S-sulfhydration in WT, but not in the C259S Stat3. These data suggest that H2S may directly regulate Cys259 residue in Stat3 and then impair its signaling function. Our data indicate that H2S may attenuate vascular calcification by upregulating elastin level through the inhibition of Stat3/CAS signaling. Full article
(This article belongs to the Special Issue Cardiovascular Complications of Diabetes)
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Review

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18 pages, 711 KiB  
Review
The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function
by Scott P. Levick and Alexander Widiapradja
Int. J. Mol. Sci. 2020, 21(3), 970; https://doi.org/10.3390/ijms21030970 - 1 Feb 2020
Cited by 36 | Viewed by 4214
Abstract
Diabetic cardiomyopathy involves remodeling of the heart in response to diabetes that includes microvascular damage, cardiomyocyte hypertrophy, and cardiac fibrosis. Cardiac fibrosis is a major contributor to diastolic dysfunction that can ultimately result in heart failure with preserved ejection fraction. Cardiac fibroblasts are [...] Read more.
Diabetic cardiomyopathy involves remodeling of the heart in response to diabetes that includes microvascular damage, cardiomyocyte hypertrophy, and cardiac fibrosis. Cardiac fibrosis is a major contributor to diastolic dysfunction that can ultimately result in heart failure with preserved ejection fraction. Cardiac fibroblasts are the final effector cell in the process of cardiac fibrosis. This review article aims to describe the cardiac fibroblast phenotype in response to high-glucose conditions that mimic the diabetic state, as well as to explain the pathways underlying this phenotype. As such, this review focuses on studies conducted on isolated cardiac fibroblasts. We also describe molecules that appear to oppose the pro-fibrotic actions of high glucose on cardiac fibroblasts. This represents a major gap in knowledge in the field that needs to be addressed. Full article
(This article belongs to the Special Issue Cardiovascular Complications of Diabetes)
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17 pages, 1936 KiB  
Review
The Changing Landscape of Pharmacotherapy for Diabetes Mellitus: A Review of Cardiovascular Outcomes
by Linda Wu and Jenny E. Gunton
Int. J. Mol. Sci. 2019, 20(23), 5853; https://doi.org/10.3390/ijms20235853 - 21 Nov 2019
Cited by 14 | Viewed by 5135
Abstract
The prevention of cardiovascular morbidity and mortality has always been a primary concern in patients with type 2 diabetes. Modern trials of glucose-lowering therapies now assess major adverse cardiac events as an endpoint in addition to the effects on glycaemic control. Whilst the [...] Read more.
The prevention of cardiovascular morbidity and mortality has always been a primary concern in patients with type 2 diabetes. Modern trials of glucose-lowering therapies now assess major adverse cardiac events as an endpoint in addition to the effects on glycaemic control. Whilst the data on the efficacy of intensive glucose lowering on reducing cardiovascular risk are limited, there are now increasing numbers of glucose-lowering therapies that have proven cardiovascular benefit independent of glucose lowering. This review will summarise the available literature on cardiovascular outcomes in relation to metformin, sulphonylureas, di-peptidyl peptidase-4 inhibitors, glucagon-like peptide receptor agonists, sodium-glucose co-transporter 2 inhibitors, thiazolidinediones, acarbose and insulin. In addition, new paradigms in diabetes management and the importance of treatment selection based on considerations including but not limited to glycaemic control will be discussed. Full article
(This article belongs to the Special Issue Cardiovascular Complications of Diabetes)
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