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Cellular and Molecular Biology of Cardiac Hypertrophy and Heart Failure: Pathogenesis, Diagnostics and Treatment—2nd Edition

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Retired, Department of Physiology and Pharmacology, University of Western Ontario, London, ON N6G 2X6, Canada
Interests: cardiac hypertrophy; heart failure; sodium hydrogen exchange (NHE1); adipokines; traditional Chinese medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will comprise a continuation of our previous Special Issue, titled “Cellular and Molecular Biology of Cardiac Hypertrophy and Heart Failure: Pathogenesis, Diagnostics and Treatment” (https://www.mdpi.com/journal/ijms/special_issues/HJJZ6ZV053).

Heart failure represents a major worldwide medical challenge in the 21st century. Although new therapeutic strategies have been developed, the incidence and mortality rates in heart failure remain high, resulting in substantial personal, emotional and financial burdens. One roadblock in effectively treating heart failure is the complexity of cellular and molecular mechanisms underlying the remodelling process.

I am pleased to announce that the International Journal of Molecular Sciences is devoting a second Special Issue to this subject, entitled "Cellular and Molecular Biology of Cardiac Hypertrophy and Heart Failure: Pathogenesis, Diagnostics and Treatment—2nd Edition". Manuscripts should be submitted in the form of research papers or review articles related to either basic or clinical research. 

Topics of interest for this Special Issue include, but are not restricted to, the following:

  • Cell signalling processes;
  • Energy metabolism;
  • Autophagy and mitophagy;
  • Apoptosis;
  • Ion (dys)regulation;
  • Mechanisms behind increased dysrhythmogenesis;
  • Adipokines;
  • Hormonal and humoral factors;
  • Novel therapeutic approaches;
  • Natural plant-based therapeutics;
  • The gut microbiome.

Prof. Dr. Morris Karmazyn
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 250 words) can be sent to the Editorial Office for assessment.

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

  • cardiac hypertrophy
  • myocardial remodelling
  • heart failure
  • cellular mechanisms
  • molecular mechanisms

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Published Papers (1 paper)

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Research

15 pages, 17231 KB  
Article
ArfGAP with Dual Pleckstrin Homology Domains 2 Promotes Hypertrophy of Cultured Neonatal Cardiomyocytes
by Jonathan Berthiaume, Audrey-Ann Dumont, Lauralyne Dumont, Marie-Frédérique Roy, Hugo Giguère and Mannix Auger-Messier
Int. J. Mol. Sci. 2025, 26(15), 7588; https://doi.org/10.3390/ijms26157588 - 6 Aug 2025
Viewed by 711
Abstract
Cardiomyocyte hypertrophy is regulated by several factors, including the ADP-ribosylation factor (Arf) family of small G proteins, among others. For instance, ArfGAP with dual pleckstrin homology domains 1 (Adap1) exerts an anti-hypertrophic effect in cultured cardiomyocytes. Its homologous protein, Adap2, is also expressed [...] Read more.
Cardiomyocyte hypertrophy is regulated by several factors, including the ADP-ribosylation factor (Arf) family of small G proteins, among others. For instance, ArfGAP with dual pleckstrin homology domains 1 (Adap1) exerts an anti-hypertrophic effect in cultured cardiomyocytes. Its homologous protein, Adap2, is also expressed in the heart but its role remains elusive. To elucidate its function, we investigated the effects of adenoviral-mediated overexpression of Adap2 in cultured neonatal rat ventricular myocytes under both basal and pro-hypertrophic conditions, employing a range of microscopy and biochemical techniques. Despite minimal detection in neonatal rat hearts, Adap2 was found to be well expressed in adult rat hearts, being predominantly localized at the membrane fraction. In contrast to Adap1, overexpression of Adap2 provokes the robust accumulation of β1-integrin at the cellular surface of cultured cardiomyocytes. Interestingly, overexpressed Adap2 relocalizes at the sarcolemma and increases the size of cardiomyocytes upon phenylephrine stimulation, despite attenuating Erk1/2 phosphorylation and Nppa gene expression. Under these same conditions, cardiomyocytes overexpressing Adap2 also express higher level of detyrosinated tubulin, a marker of hypertrophic response. These findings provide new insights into the pro-hypertrophic function of Adap2 in cardiomyocytes. Full article
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