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Special Issue "Advances in the Domain of Heart Failure"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (30 September 2021).

Special Issue Editor

Prof. Dr. Joachim Neumann
E-Mail Website
Guest Editor
Institute of Pharmacology and Toxicology, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany
Interests: dopamine; histamine; proteinphosphatases; heart failure; arrhythmias; serotonin
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Special Issue Information

Dear Colleagues,

The special issue will deal with original experimental studies on current or new or controversial issues in cardiac function. More specifically, manuscripts are solicited regarding molecular mechanisms (especially due to gene alterations) of systolic or diastolic heart failure or cardiac hypertrophy. The pharmacology of newer drugs or new aspects in the signal transduction of known drugs is of interest. Moreover, manuscripts describing new untoward i.e. toxic effects of drugs used in clinical practice would fall into the scope of this special edition. Furthermore, putative mechanism(s) of arrhythmias are of interest as far as these arrhythmias are secondary to heart failure and not primary arrhythmias. Another topic that may be addressed is the mechanism(s) of heart failure in ageing in humans or relevant ageing animal models. Experimental studies and up to date reviews of underlying mechanism of heart failure are deemed relevant. Finally, an overview and a critical perspective on drugs tested and being tested currently for heart failure will be awaited with interest.

Prof. Dr. Joachim Neumann
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 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. 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.


  • mechanism(s) heart failure
  • hypertrophy
  • pharmacology
  • new drugs
  • mechanism(s) of arrhythmias
  • ageing

Published Papers (1 paper)

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Mechanisms of Systolic Cardiac Dysfunction in PP2A, PP5 and PP2AxPP5 Double Transgenic Mice
Int. J. Mol. Sci. 2021, 22(17), 9448; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179448 - 31 Aug 2021
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As part of our ongoing studies on the potential pathophysiological role of serine/threonine phosphatases (PP) in the mammalian heart, we have generated transgenic mice with cardiac muscle cell-specific overexpression of PP2Acα (PP2A) and PP5 (PP5). For further studies we crossbred PP2A and PP5 [...] Read more.
As part of our ongoing studies on the potential pathophysiological role of serine/threonine phosphatases (PP) in the mammalian heart, we have generated transgenic mice with cardiac muscle cell-specific overexpression of PP2Acα (PP2A) and PP5 (PP5). For further studies we crossbred PP2A and PP5 mice to obtain PP2AxPP5 double transgenic mice (PP2AxPP5, DT) and compared them with littermate wild-type mice (WT) serving as a control. The mortality of DT mice was greatly enhanced vs. other genotypes. Cardiac fibrosis was noted histologically and mRNA levels of collagen 1α, collagen 3α and fibronectin 1 were augmented in DT. DT and PP2A mice exhibited an increase in relative heart weight. The ejection fraction (EF) was reduced in PP2A and DT but while the EF of PP2A was nearly normalized after β-adrenergic stimulation by isoproterenol, it was almost unchanged in DT. Moreover, left atrial preparations from DT were less sensitive to isoproterenol treatment both under normoxic conditions and after hypoxia. In addition, levels of the hypertrophy markers atrial natriuretic peptide and B-type natriuretic peptide as well as the inflammation markers interleukin 6 and nuclear factor kappa B were increased in DT. PP2A enzyme activity was enhanced in PP2A vs. WT but similar to DT. This was accompanied by a reduced phosphorylation state of phospholamban at serine-16. Fittingly, the relaxation times in left atria from DT were prolonged. In summary, cardiac co-overexpression of PP2A and PP5 were detrimental to animal survival and cardiac function, and the mechanism may involve dephosphorylation of important regulatory proteins but also fibrosis and inflammation. Full article
(This article belongs to the Special Issue Advances in the Domain of Heart Failure)
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