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Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases

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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 (20 January 2023) | Viewed by 20287

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Prof. Dr. Lih Kuo

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Department of Medical Physiology, Texas A&M University Health Science Center, Bryan, TX 77807, USA
Interests: vascular biology; cardiovascular pathophysiology; coronary ischemia; diabetic and hypertensive retinopathy; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This project aims to collect high-quality research articles, comprehensive reviews, and novel communications on fundamental and molecular researches on all kinds of cardiovascular and cerebrovascular diseases. We encourage the submission of manuscripts which provide novel and mechanistic insights and papers that report significant advances in the field.

The topics of interest for this Special Issue include, but are not limited to, the following:

Aneurysms;
Aortic disease;
Cerebrovascular disease;
Congenital heart disease;
Coronary/cerebral artery disease;
Coronary/cerebral ischemia;
Coronary/cerebral thrombosis;
Deep vein thrombosis;
Genetic cardiovascular/cerebrovascular disease;
Heart attack;
Heart failure;
Heart muscle disease;
Heart valve disease;
Lymphatic pathophysiology;
Microvascular disorder;
Pericardial disease;
Peripheral vascular disease;
Rheumatic heart disease;
Stroke;
Transient ischemic attack;
(repetitive)Vascular remodeling/dysfunction/malformation.

The investigations we will focus our attention on are fundamentally cellular/molecular studies, although scientific articles that incorporate clinical data in addition to cellular/molecular studies will be similarly accepted.

Prof. Dr. Lih Kuo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

cardiovascular diseases
cerebrovascular diseases
cardio-neuro-vascular
molecular pathology

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Published Papers (6 papers)

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Research

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10 pages, 3154 KiB

Open AccessArticle

The Effect of Anti-Autotaxin Aptamers on the Development of Proliferative Vitreoretinopathy

by Hirotsugu Hanazaki, Harumasa Yokota, Satoru Yamagami, Yoshikazu Nakamura and Taiji Nagaoka

Int. J. Mol. Sci. 2023, 24(21), 15926; https://doi.org/10.3390/ijms242115926 - 3 Nov 2023

Viewed by 1318

Abstract

This study investigated the effect of anti-autotaxin (ATX) aptamers on the development of proliferative vitreoretinopathy (PVR) in both in vivo and in vitro PVR swine models. For the in vitro study, primary retinal pigment epithelial (RPE) cells were obtained from porcine eyes and cultured for cell proliferation and migration assays. For the in vivo study, a swine PVR model was established by inducing retinal detachment and injecting cultured RPE cells (2.0 × 10⁶). Concurrently, 1 week after RPE cell injection, the anti-ATX aptamer, RBM-006 (10 mg/mL, 0.1 mL), was injected twice into the vitreous cavity. Post-injection effects of the anti-ATX aptamer on PVR development in the in vivo swine PVR model were investigated. For the in vitro evaluation, the cultured RPE cell proliferation and migration were significantly reduced at anti-ATX aptamer concentrations of 0.5–0.05 mg and at only 0.5 mg, respectively. Intravitreal administration of the anti-ATX aptamer also prevented tractional retinal detachment caused by PVR in the in vivo PVR model. We observed that the anti-ATX aptamer, RBM-006, inhibited PVR-related RPE cell proliferation and migration in vitro and inhibited the progression of PVR in the in vivo model, suggesting that the anti-ATX aptamer may be effective in preventing PVR. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases)

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17 pages, 5696 KiB

Open AccessArticle

Smooth Muscle-Alpha Actin R149C Pathogenic Variant Downregulates Integrin Recruitment at Cell-Matrix Adhesions and Decreases Cellular Contractility

by Krishna R. Ojha, Hyoseon Kim, Samuel Padgham, Laura Hopkins, Robert J. Zamen, Abhijnan Chattopadhyay, Gang Han, Dianna M. Milewicz, Michael P. Massett and Andreea Trache

Int. J. Mol. Sci. 2023, 24(11), 9616; https://doi.org/10.3390/ijms24119616 - 1 Jun 2023

Cited by 3 | Viewed by 1856

Abstract

Thoracic aortic aneurysm is found in patients with ACTA2 pathogenic variants. ACTA2 missense variants are associated with impaired aortic smooth muscle cell (SMC) contraction. This study tested the hypothesis that the Acta2^R149C/+ variant alters actin isoform expression and decreases integrin recruitment, thus, reducing aortic contractility. Stress relaxation measurements in thoracic aortic rings showed two functional regimes with a reduction of stress relaxation in the aorta from Acta2^R149C/+ mice at low tension, but not at high tension values. Contractile responses to phenylephrine and potassium chloride were 50% lower in Acta2^R149C/+ mice than in wild-type (WT) mice. Additionally, SMC were immunofluorescently labeled for specific proteins and imaged by confocal or total internal reflection fluorescence microscopy. The quantification of protein fluorescence of Acta2^R149C/+ SMC showed a downregulation in smooth muscle α-actin (SMα-actin) and a compensatory upregulation of smooth muscle γ-actin (SMγ-actin) compared to WT cells. These results suggest that downregulation of SMα-actin leads to reduced SMC contractility, while upregulation of SMγ-actin may lead to increased SMC stiffness. Decreased α5β1 and α2β1 integrin recruitment at cell-matrix adhesions further reduce the ability of mutant cells to participate in cell-matrix crosstalk. Collectively, the results suggest that mutant Acta2^R149C/+ aortic SMC have reduced contractility and interaction with the matrix, which are potential long-term contributing factors to thoracic aortic aneurysms. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases)

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15 pages, 2201 KiB

Open AccessArticle

H₂O₂ Mediates VEGF- and Flow-Induced Dilations of Coronary Arterioles in Early Type 1 Diabetes: Role of Vascular Arginase and PI3K-Linked eNOS Uncoupling

by Naris Thengchaisri, Lih Kuo and Travis W. Hein

Int. J. Mol. Sci. 2023, 24(1), 489; https://doi.org/10.3390/ijms24010489 - 28 Dec 2022

Cited by 2 | Viewed by 1930

Abstract

In diabetes, the enzyme arginase is upregulated, which may compete with endothelial nitric oxide (NO) synthase (eNOS) for their common substrate L-arginine and compromise NO-mediated vasodilation. However, this eNOS uncoupling can lead to superoxide production and possibly vasodilator hydrogen peroxide (H₂O₂) formation to compensate for NO deficiency. This hypothesis was tested in coronary arterioles isolated from pigs with 2-week diabetes after streptozocin injection. The NO-mediated vasodilation induced by flow and VEGF was abolished by NOS inhibitor L-NAME and phosphoinositide 3-kinase (PI3K) inhibitor wortmannin but was not affected by arginase inhibitor N^ω-hydroxy-nor-L-arginine (nor-NOHA) or H₂O₂ scavenger catalase in control pigs. With diabetes, this vasodilation was partially blunted, and the remaining vasodilation was abolished by catalase and wortmannin. Administration of L-arginine or nor-NOHA restored flow-induced vasodilation in an L-NAME sensitive manner. Diabetes did not alter vascular superoxide dismutase 1, catalase, and glutathione peroxidase mRNA levels. This study demonstrates that endothelium-dependent NO-mediated coronary arteriolar dilation is partially compromised in early type 1 diabetes by reducing eNOS substrate L-arginine via arginase activation. It appears that upregulated arginase contributes to endothelial NO deficiency in early diabetes, but production of H₂O₂ during PI3K-linked eNOS uncoupling likely compensates for and masks this disturbance. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases)

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12 pages, 1361 KiB

Open AccessArticle

Exposure of Mice to Thirdhand Smoke Modulates In Vitro and In Vivo Platelet Responses

by Daniel Villalobos-García, Hamdy E. A. Ali, Ahmed B. Alarabi, Medhat S. El-Halawany, Fatima Z. Alshbool and Fadi T. Khasawneh

Int. J. Mol. Sci. 2022, 23(10), 5595; https://doi.org/10.3390/ijms23105595 - 17 May 2022

Cited by 5 | Viewed by 2233

Abstract

Smoking is a risk factor for a variety of deleterious conditions, such as cancer, respiratory disease and cardiovascular disease. Thrombosis is an important and common aspect of several cardiovascular disease states, whose risk is known to be increased by both first- and secondhand smoke. More recently, the residual cigarette smoke that persists after someone has smoked (referred to as thirdhand smoke or THS) has been gaining more attention, since it has been shown that it also negatively affects health. Indeed, we have previously shown that 6-month exposure to THS increases the risk of thrombogenesis. However, neither the time-dependence of THS-induced thrombus formation, nor its sex dependence have been investigated. Thus, in the present study, we investigated these issues in the context of a shorter exposure to THS, specifically 3 months, in male and female mice. We show that the platelets from 3-month THS-exposed mice exhibited enhanced activation by agonists. Moreover, we also show that mice of both sexes exposed to THS have decreased tail bleeding as well as decreased thrombus occlusion time. In terms of the role of sex, intersex disparities in thrombus development and hemostasis as well as in platelet aggregation were, interestingly, observed. Together, our findings show that exposing mice to THS for 3 months is sufficient to predispose them to thrombosis; which seems to be driven, at least in part, by an increased activity in platelets, and that it does not manifest equally in both sexes. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases)

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Review

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18 pages, 692 KiB

Open AccessReview

The Tissue Response to Hypoxia: How Therapeutic Carbon Dioxide Moves the Response toward Homeostasis and Away from Instability

by Richard J. Rivers and Cynthia J. Meininger

Int. J. Mol. Sci. 2023, 24(6), 5181; https://doi.org/10.3390/ijms24065181 - 8 Mar 2023

Cited by 8 | Viewed by 8926

Abstract

Sustained tissue hypoxia is associated with many pathophysiological conditions, including chronic inflammation, chronic wounds, slow-healing fractures, microvascular complications of diabetes, and metastatic spread of tumors. This extended deficiency of oxygen (O₂) in the tissue sets creates a microenvironment that supports inflammation and initiates cell survival paradigms. Elevating tissue carbon dioxide levels (CO₂) pushes the tissue environment toward “thrive mode,” bringing increased blood flow, added O₂, reduced inflammation, and enhanced angiogenesis. This review presents the science supporting the clinical benefits observed with the administration of therapeutic CO₂. It also presents the current knowledge regarding the cellular and molecular mechanisms responsible for the biological effects of CO₂ therapy. The most notable findings of the review include (a) CO₂ activates angiogenesis not mediated by hypoxia-inducible factor 1a, (b) CO₂ is strongly anti-inflammatory, (c) CO₂ inhibits tumor growth and metastasis, and (d) CO₂ can stimulate the same pathways as exercise and thereby, acts as a critical mediator in the biological response of skeletal muscle to tissue hypoxia. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases)

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21 pages, 1506 KiB

Open AccessReview

MicroRNA-150 (miR-150) and Diabetic Retinopathy: Is miR-150 Only a Biomarker or Does It Contribute to Disease Progression?

by Gladys Y.-P. Ko, Fei Yu, Kayla J. Bayless and Michael L. Ko

Int. J. Mol. Sci. 2022, 23(20), 12099; https://doi.org/10.3390/ijms232012099 - 11 Oct 2022

Cited by 9 | Viewed by 3042

Abstract

Diabetic retinopathy (DR) is a chronic disease associated with diabetes mellitus and is a leading cause of visual impairment among the working population in the US. Clinically, DR has been diagnosed and treated as a vascular complication, but it adversely impacts both neural retina and retinal vasculature. Degeneration of retinal neurons and microvasculature manifests in the diabetic retina and early stages of DR. Retinal photoreceptors undergo apoptosis shortly after the onset of diabetes, which contributes to the retinal dysfunction and microvascular complications leading to vision impairment. Chronic inflammation is a hallmark of diabetes and a contributor to cell apoptosis, and retinal photoreceptors are a major source of intraocular inflammation that contributes to vascular abnormalities in diabetes. As the levels of microRNAs (miRs) are changed in the plasma and vitreous of diabetic patients, miRs have been suggested as biomarkers to determine the progression of diabetic ocular diseases, including DR. However, few miRs have been thoroughly investigated as contributors to the pathogenesis of DR. Among these miRs, miR-150 is downregulated in diabetic patients and is an endogenous suppressor of inflammation, apoptosis, and pathological angiogenesis. In this review, how miR-150 and its downstream targets contribute to diabetes-associated retinal degeneration and pathological angiogenesis in DR are discussed. Currently, there is no effective treatment to stop or reverse diabetes-caused neural and vascular degeneration in the retina. Understanding the molecular mechanism of the pathogenesis of DR may shed light for the future development of more effective treatments for DR and other diabetes-associated ocular diseases. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cardiovascular and Cerebrovascular Diseases)

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