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Cells
Special Issues
Molecular and Cellular Mechanisms of Cardiovascular and Metabolic Diseases
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Molecular and Cellular Mechanisms of Cardiovascular and Metabolic Diseases

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 1688

Special Issue Editor

Dr. Prathapan Ayyappan

E-Mail Website
Guest Editor
1. Environmental Influences on Health and Disease Group, Sanford Research, Sioux Falls, SD 57104, USA
2. Department of Pediatrics, Sanford School of Medicine, University of South Dakota, Sioux Falls, SD, USA
Interests: mitochondrial dysfunction; endoplasmic reticulum (ER) stress; oxidative/nitrosative stress; atherosclerosis; metabolomics; cell death

Special Issue Information

Dear Colleagues,

Globally, cardiovascular disease (CVD) is the leading cause of death, the primary contributor to disability, and causes about one third of all deaths. The prevalence of and disability due to CVD has doubled and is affecting more than 500 million people. CVD is influenced by both environmental and genetic triggers. Even though there is significant progress in identifying the multifactorial mechanisms associated with cardiometabolic complications; studies are still needed to unravel novel molecular mechanisms that may open new therapeutic horizons and will significantly reduce the prevalence and disability associated with this disease. This Special Issue focuses on the pathophysiology and novel molecular mechanism associated with cardiometabolic syndrome with a special emphasis on mitochondrial dysfunction, ER stress, oxidative stress, obesity, diabetes, anticancer drug-mediated cardiomyopathy, atherosclerosis, and nutrition. Identifying novel molecular mechanisms may help to implement cost effective, population-based early prevention.

Dr. Prathapan Ayyappan
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. 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

  • mitochondrial dysfunction
  • endoplasmic reticulum (ER) stress
  • oxidative/nitrosative stress
  • diabetes
  • obesity
  • diet
  • atherosclerosis
  • hypertension
  • metabolomics
  • cell death
  • nutraceuticals/functional foods

Published Papers (1 paper)

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Research

17 pages, 3391 KiB  
Article
Dose-Dependent Effects of Radiation on Mitochondrial Morphology and Clonogenic Cell Survival in Human Microvascular Endothelial Cells
by Li Wang, Rafael Rivas, Angelo Wilson, Yu Min Park, Shannon Walls, Tianzheng Yu and Alexandra C. Miller
Cells 2024, 13(1), 39; https://doi.org/10.3390/cells13010039 - 23 Dec 2023
Viewed by 1118
Abstract
To better understand radiation-induced organ dysfunction at both high and low doses, it is critical to understand how endothelial cells (ECs) respond to radiation. The impact of irradiation (IR) on ECs varies depending on the dose administered. High doses can directly damage ECs, [...] Read more.
To better understand radiation-induced organ dysfunction at both high and low doses, it is critical to understand how endothelial cells (ECs) respond to radiation. The impact of irradiation (IR) on ECs varies depending on the dose administered. High doses can directly damage ECs, leading to EC impairment. In contrast, the effects of low doses on ECs are subtle but more complex. Low doses in this study refer to radiation exposure levels that are below those that cause immediate and necrotic damage. Mitochondria are the primary cellular components affected by IR, and this study explored their role in determining the effect of radiation on microvascular endothelial cells. Human dermal microvascular ECs (HMEC-1) were exposed to varying IR doses ranging from 0.1 Gy to 8 Gy (~0.4 Gy/min) in the AFRRI 60-Cobalt facility. Results indicated that high doses led to a dose-dependent reduction in cell survival, which can be attributed to factors such as DNA damage, oxidative stress, cell senescence, and mitochondrial dysfunction. However, low doses induced a small but significant increase in cell survival, and this was achieved without detectable DNA damage, oxidative stress, cell senescence, or mitochondrial dysfunction in HMEC-1. Moreover, the mitochondrial morphology was assessed, revealing that all doses increased the percentage of elongated mitochondria, with low doses (0.25 Gy and 0.5 Gy) having a greater effect than high doses. However, only high doses caused an increase in mitochondrial fragmentation/swelling. The study further revealed that low doses induced mitochondrial elongation, likely via an increase in mitochondrial fusion protein 1 (Mfn1), while high doses caused mitochondrial fragmentation via a decrease in optic atrophy protein 1 (Opa1). In conclusion, the study suggests, for the first time, that changes in mitochondrial morphology are likely involved in the mechanism for the radiation dose-dependent effect on the survival of microvascular endothelial cells. This research, by delineating the specific mechanisms through which radiation affects endothelial cells, offers invaluable insights into the potential impact of radiation exposure on cardiovascular health. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular and Metabolic Diseases)
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