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Advanced Communications in Cardiovascular Disease: Small Vesicles and Cell Identity...
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Advanced Communications in Cardiovascular Disease: Small Vesicles and Cell Identity Theft

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (25 October 2022) | Viewed by 9050

Special Issue Editors

Dr. Yajing Wang

E-Mail Website
Guest Editor
Emergency Medicine Department, Thomas Jefferson University, College Building 300, State College, PA 19107, USA
Interests: ischemia-reperfusion; AMPK; autophagy; Caveolin; diabetes; miRNA; extracellular vesicles; apoptosis; heart failure; microvascular circulation; endothelial dysfunction
Prof. Dr. William Chilian

E-Mail Website
Guest Editor
Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA
Interests: regulatory mechanisms in coronary microcirculation; coronary angiogenesis and arteriogenesis; non-linear behavior of biological systems; mechanosensitive gene expression and signal transduction; redox regulation of ion channel function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The interactions between metabolic organs have evolved concomitantly to maintain whole-body energy homeostasis and ensure the organism’s adaption to external cues. Extracellular vesicles and intracellular vesicles are emerging as a new category of messengers that facilitate crosstalk among organs and within cells. Dynamic movement of the small vesicles is the basis of maintaining internal environment stabilization. Small vesicles play a pivotal role in various cardiovascular diseases, including diabetic cardiomyopathy. Macroautophagy (classic autophagy) in particular is an evolutionarily conserved mechanism for the maintenance of physiological homeostasis and balancing energies in reusage and expenditure. As energy resources, mitochondria are essential to cardiovascular homeostasis in health. Maintaining a healthy mitochondrial balance and rebalancing dysfunctional mitochondria quality and quantity are involved in various therapeutic strategies. 

In order to develop new insights into the intimate connection between small vesicles, including small extracellular vesicles, and intracellular vesicle movement in cardiovascular disorders, we will introduce the genetic and epigenetic role of regulatory factors and maneuvers that alter extra-/intracellular communication in various types of cardiomyopathy and in cardiovascular diseases.

This Special Issue entitled “Advanced Communications in Cardiovascular Disease: Small Vesicles and Cell Identity Ttheft” welcomes manuscripts from original investigations and comprehensive reviews demonstrating new and advanced research viewpoints on the mechanisms of regulating inter-/intracellular communications to cardiovascular disease with or without diabetes.

Dr. Yajing Wang
Prof. Dr. William Chilian
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • microvascular circulation
  • metabolism
  • autophagy
  • diabetes
  • epigenetic regulation
  • vesicles
  • endothelial dysfunction
  • cardiovascular disease

Published Papers (3 papers)

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Research

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15 pages, 4375 KiB  
Article
Withaferin a Attenuates Retinal Ischemia-Reperfusion Injury via Akt-Dependent Inhibition of Oxidative Stress
by Zheyi Yan, Yuanlin Zhang, Chunfang Wang, Yanjie Li, Qiang Su, Jimin Cao and Xiaoming Cao
Cells 2022, 11(19), 3113; https://doi.org/10.3390/cells11193113 - 02 Oct 2022
Cited by 5 | Viewed by 1557
Abstract
Background: Retinal ischemia-reperfusion (I/R) injury often results in intractable visual impairments. The survival of retinal capillary endothelial cells is crucial for the treatment of retinal I/R injury. How to protect retinal endothelia from damage is a challenging work. Withaferin A, a small molecule [...] Read more.
Background: Retinal ischemia-reperfusion (I/R) injury often results in intractable visual impairments. The survival of retinal capillary endothelial cells is crucial for the treatment of retinal I/R injury. How to protect retinal endothelia from damage is a challenging work. Withaferin A, a small molecule derived from plants, has antibacterial and anti-inflammatory effects and has been used for about millennia in traditional medicine. The present study aimed to investigate the potential protective effect of withaferin A on retinal I/R injury. Methods: The drug-likeness of withaferin A was evaluated by the SwissADME web tool. The potential protective effect of withaferin A on the I/R-induced injury of human retinal microvascular endothelial cells (HRMECs) was investigated using multiple approaches. RNA sequencing was performed and associated mechanistic signaling pathways were analyzed based on the Kyoto Encyclopedia of Genes and Genomes data. The analytical results of RNA sequencing data were further validated by in vitro and in vivo experiments. Results: Withaferin A reduced the I/R injury-induced apoptotic death of HRMECs in vitro with a good drug-like property. RNA sequencing and experimental validation results indicated that withaferin A increased the production of the crucial antioxidant molecules heme oxygenase 1 (HO-1) and peroxiredoxin 1 (Prdx-1) during I/R. In addition, withaferin A activated the Akt signaling pathway and increased the expression of HO-1 and Prdx-1, thereby exerting an antioxidant effect, attenuated the retinal I/R injury, and decreased the apoptosis of HRMECs. The blockade of Akt completely abolished the effects of withaferin A. Conclusions: The study identified for the first time that withaferin A can protect against the I/R-induced apoptosis of human microvascular retinal endothelial cells via increasing the production of the antioxidants Prdx-1 and HO-1. Results suggest that withaferin A is a promising drug candidate for the treatment of retinal I/R injury. Full article
(This article belongs to the Special Issue Advanced Communications in Cardiovascular Disease: Small Vesicles and Cell Identity Theft)
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Review

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19 pages, 1191 KiB  
Review
Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management
by Jinjuan Yang, Shaoxiang Chen, Fuyu Duan, Xiuxiu Wang, Xiaoxian Zhang, Boonxuan Lian, Meng Kou, Zhixin Chiang, Ziyue Li and Qizhou Lian
Cells 2022, 11(21), 3511; https://doi.org/10.3390/cells11213511 - 06 Nov 2022
Cited by 5 | Viewed by 2742
Abstract
Mitochondrial cardiomyopathy (MCM) is characterized by abnormal heart-muscle structure and function, caused by mutations in the nuclear genome or mitochondrial DNA. The heterogeneity of gene mutations and various clinical presentations in patients with cardiomyopathy make its diagnosis, molecular mechanism, and therapeutics great challenges. [...] Read more.
Mitochondrial cardiomyopathy (MCM) is characterized by abnormal heart-muscle structure and function, caused by mutations in the nuclear genome or mitochondrial DNA. The heterogeneity of gene mutations and various clinical presentations in patients with cardiomyopathy make its diagnosis, molecular mechanism, and therapeutics great challenges. This review describes the molecular epidemiology of MCM and its clinical features, reviews the promising diagnostic tests applied for mitochondrial diseases and cardiomyopathies, and details the animal and cellular models used for modeling cardiomyopathy and to investigate disease pathogenesis in a controlled in vitro environment. It also discusses the emerging therapeutics tested in pre-clinical and clinical studies of cardiac regeneration. Full article
(This article belongs to the Special Issue Advanced Communications in Cardiovascular Disease: Small Vesicles and Cell Identity Theft)
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19 pages, 1789 KiB  
Review
Endothelial Autophagy in Coronary Microvascular Dysfunction and Cardiovascular Disease
by Fujie Zhao, Ganesh Satyanarayana, Zheng Zhang, Jianli Zhao, Xin-Liang Ma and Yajing Wang
Cells 2022, 11(13), 2081; https://doi.org/10.3390/cells11132081 - 30 Jun 2022
Cited by 8 | Viewed by 3994
Abstract
Coronary microvascular dysfunction (CMD) refers to a subset of structural and/or functional disorders of coronary microcirculation that lead to impaired coronary blood flow and eventually myocardial ischemia. Amid the growing knowledge of the pathophysiological mechanisms and the development of advanced tools for assessment, [...] Read more.
Coronary microvascular dysfunction (CMD) refers to a subset of structural and/or functional disorders of coronary microcirculation that lead to impaired coronary blood flow and eventually myocardial ischemia. Amid the growing knowledge of the pathophysiological mechanisms and the development of advanced tools for assessment, CMD has emerged as a prevalent cause of a broad spectrum of cardiovascular diseases (CVDs), including obstructive and nonobstructive coronary artery disease, diabetic cardiomyopathy, and heart failure with preserved ejection fraction. Of note, the endothelium exerts vital functions in regulating coronary microvascular and cardiac function. Importantly, insufficient or uncontrolled activation of endothelial autophagy facilitates the pathogenesis of CMD in diverse CVDs. Here, we review the progress in understanding the pathophysiological mechanisms of autophagy in coronary endothelial cells and discuss their potential role in CMD and CVDs. Full article
(This article belongs to the Special Issue Advanced Communications in Cardiovascular Disease: Small Vesicles and Cell Identity Theft)
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