Special Issue "Nutrient Deficiency and Drug Induced Cardiac Injury and Dysfunction"
A special issue of Hearts (ISSN 2673-3846).
Deadline for manuscript submissions: 1 September 2020.
Interests: cardiovascular injury and dysfunction; contribution of Mg deficiency; roles of anti-retroviral drugs and anti-cancer EGFR-TKIs; lysosomal iron and effects of beta-blockers; neurogenic inflammation; intervention by SP-receptor blockade; oxidative/nitrosative stress; glutathione status; genomic regulation of the Nrf2 pathway
Interests: free radicals [reactive oxygen/nitrogen species]; free radical spin trapping; antioxidants; adverse side effects of anti-cancer EGFR-tyrosine kinase inhibitors; lipid peroxidation; experimental cardiac ischemia-reperfusion injury and dysfunction; iron overload; magnesium deficiency; neurogenic inflammation and use of substance P receptor antagonists; experimental echocardiography
Cardiac injury manifested as either systolic or diastolic dysfunction is considered an important preceding stage leading to or associated with eventual heart failure. There is increasing literature recognizing that deficiency and/or imbalance of certain essential micronutrients, vitamins, and macrominerals may be involved in the pathogenesis of cardiomyopathy/injury/contractile dysfunction. Essential micronutrients may include, but not limited to, water soluble B vitamins such as thiamine, vitamin C, fat-soluble vitamins (A, E, D, K), carnitine, Coenzyme Q10, and taurine (a conditionally essential amino acid), as well as microminerals, such as selenium, zinc, copper, cobalt, and chromium. Notable macrominerals may include magnesium, calcium, iron, and potassium. While much of the nutritional deficiency might be caused by poor dietary intake, certain nutrient deficiencies, especially of Mg leading to hypomagnesemia, may be caused by excessive alcohol intake, antiretroviral drug treatments of HIV/AIDS patients, or anticancer therapeutics such as epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) and cisplatin. Anticancer drugs may cause kidney injury and dysfunction, leading to malabsorption of Mg and renal Mg wasting. Many of the listed micronutrients are co-factors of metabolic reactions, and their deficiency would disturb myocardial substrate metabolism and energy utilization. Mg plays a key role in modulating neuronal excitation, endothelial function, and cardiac contraction by regulating several ion channels, including K and Ca; Mg is also a key co-factor for mitochondrial ATP production. As such, Mg deficiency may contribute to the pathogenesis of cardiac arrhythmias and dysfunction. Iron can be a pro-oxidant mineral, but iron is essential for the development of normal red blood cells and healthy immune function, and its deficiency is the most widespread nutritional deficiency in the world.
While it remains unclear if any chronic nutrient deficiency-induced cardiac injury/dysfunction is readily reversible, no consistent nutritional supplementation has been recommended as a rescue strategy against cardiac injury/dysfunction. It is noted that many of the micronutrients have antioxidant properties (e.g., vitamins E and C, selenium, and Coenzyme Q10). Mg is a natural calcium blocker, and its elevated intake above normal levels may also produce antioxidative, anti-inflammatory effects in vivo. The purpose of this Special Issue is to provide a platform for recent experimental or clinical research that may shed new light on nutrient/mineral deficiencies or adverse drug effects that may impair cardiac function directly or indirectly. Common mechanistic parameters may involve systemic oxidative/nitrosative stress, neurogenic inflammation, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, oxidative/antioxidant gene up-regulation, and/or compromised antioxidant defenses, which may serve as prognostic mediators/events linked to induced cardiac injury/dysfunction. The ultimate goal is to search for a better understanding of the complex interactions and molecular mechanisms contributing to cardiac injury/dysfunction and potential effective mitigating interventions.
Prof. Dr. I.Tong Mak
Prof. Dr. Jay H. Kramer
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 papers will be 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. Hearts is an international peer-reviewed open access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. 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.
- Cardiac injury/contractile dysfunction
- Micronutrient deficiency
- Macromineral deficiency or imbalance
- Impact by cardiovascular and/or anti-cancer drugs
- Systemic inflammation
- Oxidative/nitrosative stress
- Antioxidant defenses
- Supplement and/or pathway interventions
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Vitamin A as a transcriptional regulator of cardiovascular disease
Authors: Bogac Kaynak
Affiliation: University of Helsinki
Abstract: Vitamin A is a micronutrient and signaling molecule that regulates transcription, cellular differentiation, and organ homeostasis. Additionally, metabolites of Vitamin A are utilized as differentiation agents in the treatment of hematological cancers and skin disorders, necessitating further study into the effects of both nutrient deficiency and the exogenous delivery of Vitamin A and its metabolites on cardiovascular phenotypes. Though Vitamin A is a well-known regulator of cardiac formation, recent evidence has emerged supporting its role as a regulator of postnatal cardiac function and cardiovascular disease progression. We here review findings from genetic and pharmacological studies describing the regulation of both vascular- and myocyte-driven cardiac phenotypes by Vitamin A signaling. We highlight the interaction of Vitamin A signaling with core cardiac transcription factors GATA4 and TBX5, known drivers of heart failure progression and atrial fibrillation, respectively. Finally, we pinpoint positive and negative feedback mechanisms critical to the regulation of Vitamin A signaling at both an organismal and cellular level.