Heart Failure: New Horizons in Its Pathomechanism and Treatment
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 (29 February 2024) | Viewed by 2179
Special Issue Editor
Special Issue Information
Dear Colleagues,
Heart failure is an extremely severe and complex syndrome that is pathophysiologically caused by the over-activation of three pillars: the renin–angiotensin–aldosterone system, the sympathetic nervous system, and inflammation. Although extensive research has been conducted regarding the development of therapeutic approaches for this problem, the morbidity and mortality rate remains high. According to current guidelines, the contemporaneous application of the angiotensin-converting enzyme inhibitor, the angiotensin-receptor blocker, the angiotensin receptor–neprilysin inhibitor, Beta-blocker, the mineralocorticoid receptor antagonist and Dapagliflozin/Empagliflozin must be employed. Although there has been a reduction in the hospitalization and morbidity rate, it remains high; thus, the enigma of heart failure has not been solved. In this respect, it is urgent that new pathways are searched for in order to obtain a holistic therapy for patients with chronic heart failure.
The gut microbiota is an emerging ‘organ’ that can interact with the human homeostatic system, including its metabolic state, inflammation, neurohumoral and drug resistance, etc. Therefore, we should pay attention to and endeavor to understand this emerging pathway. Indeed, it is well known that exercise and the Mediterranean diet affect the gut microbiota in a positive way, thus protecting the cardiovascular system and reducing the prevalence of cardiovascular disease.
Ultimately, heart failure is caused by a lack of energy. Energy is contributed by the mitochondria, organelles that merit our attention and research. The organelles involved in energy production are a source of free radical production and unfolded proteins, and the promotion of inflammation. Accordingly, inflammation and heart failure are intimately related, and the addition of novel therapeutic paths is necessary. Thus, if we can obtain knowledge pertaining to these new pathways, we can hope to discover novel therapeutic horizons and enhance treatment for our patients.
Prof. Dr. Ioannis A. Paraskevaidis
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
- arrhythmias
- cardiology
- angiotensin
- cardiovascular disease
- mitochondria
- inflammation
- heart failure
