Special Issue "Cardiac Growth Control and Heart Cell Death"
Deadline for manuscript submissions: closed (5 September 2022) | Viewed by 23649
Interests: mitochondria; cell death; apoptosis; necrosis; autophagy; metabolism; ischemia-reperfusion; hypoxia; nuclear factor-kappa beta; heart failure
The adult heart has a limited capacity for de novo cardiac myocyte regeneration and/or self-renewal after injury. Heart disease is the most common cause of death worldwide, and programmed cell death is postulated as a central underlying cause of ventricular remodeling and heart failure. The mitochondrion has emerged as a central platform for regulating signaling events that govern cell growth, apoptosis, necrosis and quality control mechanisms by autophagy. These highly coordinated cellular processes share common and overlapping pathways; however, the intersection of how these pathways underlie cardiac dysfunction and disease pathogenesis remains poorly understood. Therefore, studies directed toward understanding the genetic, molecular and cellular mechanisms that underlie cardiac growth and programmed cell death in the heart are of paramount importance toward the ultimate therapeutic goal of developing new therapies that will prevent cardiovascular disease. Furthermore, there is growing appreciation that the incidence and severity of heart disease are different among women and men, with the prevalence of catastrophic outcomes following myocardial infarction dependent on the body’s biological clock and circadian rhythms.
Cells will publish a Special Issue in spring 2022 titled “Cardiac Growth Control and Heart Cell Death” that will solicit original research articles and reviews highlighting new exciting findings in the area of cardiac growth control and cell death. These exciting and innovative studies will have profound clinical implications for understanding the signaling mechanisms that underlie cell death following cardiac injury. We invite submissions of novel, exciting research on broad topics in cardiovascular health and disease, including, but not limited to, autophagy, cell death, mitochondrial quality control, women's heart health, circadian-regulated cardiac function and genetic studies on approaches related to cardiovascular disease mechanisms and potential therapies. Each submitted manuscript will go through a rigorous peer-review process. Submitted manuscripts must not have been published previously nor be under consideration for publication in other journals.
Prof. Dr. Lorrie Kirshenbaum
Dr. Inna Rabinovich-Nikitin
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.
- cell death
- cardiac injury
- cardiac metabolism
- women heart health
- circadian rhythm