For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
26
views
122
references
 Top references
cited by
58
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      332
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Physiological and unappreciated roles of CaMKII in the heart

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          In the cardiomyocyte, CaMKII has been identified as a nodal influencer of excitation–contraction and also excitation–transcription coupling. Its activity can be regulated in response to changes in intracellular calcium content as well as after several post-translational modifications. Some of the effects mediated by CaMKII may be considered adaptive, while effects of sustained CaMKII activity may turn into the opposite and are detrimental to cardiac integrity and function. As such, CaMKII has long been noted as a promising target for pharmacological inhibition, but the ubiquitous nature of CaMKII has made it difficult to target CaMKII specifically where it is detrimental. In this review, we provide a brief overview of the physiological and pathophysiological properties of CaMKII signaling, but we focus on the physiological and adaptive functions of CaMKII. Furthermore, special consideration is given to the emerging role of CaMKII as a mediator of inflammatory processes in the heart.

          Related collections

          Most cited references122

          • Record: found
          • Abstract: found
          • Article: not found

          Chagas disease

          Jose Pérez-Molina, Israel Molina (2018)
          Chagas disease is an anthropozoonosis from the American continent that has spread from its original boundaries through migration. It is caused by the protozoan Trypanosoma cruzi, which was identified in the first decade of the 20th century. Once acute infection resolves, patients can develop chronic disease, which in up to 30-40% of cases is characterised by cardiomyopathy, arrhythmias, megaviscera, and, more rarely, polyneuropathy and stroke. Even after more than a century, many challenges remain unresolved, since epidemiological control and diagnostic, therapeutic, and prognostic methods must be improved. In particular, the efficacy and tolerability profile of therapeutic agents is far from ideal. Furthermore, the population affected is older and more complex (eg, immunosuppressed patients and patients with cancer). Nevertheless, in recent years, our knowledge of Chagas disease has expanded, and the international networking needed to change the course of this deadly disease during the 21st century has begun.
          Article 0 comments Cited 327 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Predicting survival in heart failure: a risk score based on 39 372 patients from 30 studies.

            Rebecca McMurray, C Ariti, Gillian A. Whalley … (2013)
            Using a large international database from multiple cohort studies, the aim is to create a generalizable easily used risk score for mortality in patients with heart failure (HF). The MAGGIC meta-analysis includes individual data on 39 372 patients with HF, both reduced and preserved left-ventricular ejection fraction (EF), from 30 cohort studies, six of which were clinical trials. 40.2% of patients died during a median follow-up of 2.5 years. Using multivariable piecewise Poisson regression methods with stepwise variable selection, a final model included 13 highly significant independent predictors of mortality in the following order of predictive strength: age, lower EF, NYHA class, serum creatinine, diabetes, not prescribed beta-blocker, lower systolic BP, lower body mass, time since diagnosis, current smoker, chronic obstructive pulmonary disease, male gender, and not prescribed ACE-inhibitor or angiotensin-receptor blockers. In preserved EF, age was more predictive and systolic BP was less predictive of mortality than in reduced EF. Conversion into an easy-to-use integer risk score identified a very marked gradient in risk, with 3-year mortality rates of 10 and 70% in the bottom quintile and top decile of risk, respectively. In patients with HF of both reduced and preserved EF, the influences of readily available predictors of mortality can be quantified in an integer score accessible by an easy-to-use website www.heartfailurerisk.org. The score has the potential for widespread implementation in a clinical setting.
            Article 0 comments Cited 264 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              RBM20, a gene for hereditary cardiomyopathy, regulates titin splicing.

              Wei. Guo, Sebastian Schafer, Marion L. Greaser … (2012)
              Alternative splicing has a major role in cardiac adaptive responses, as exemplified by the isoform switch of the sarcomeric protein titin, which adjusts ventricular filling. By positional cloning using a previously characterized rat strain with altered titin mRNA splicing, we identified a loss-of-function mutation in the gene encoding RNA binding motif protein 20 (Rbm20) as the underlying cause of pathological titin isoform expression. The phenotype of Rbm20-deficient rats resembled the pathology seen in individuals with dilated cardiomyopathy caused by RBM20 mutations. Deep sequencing of the human and rat cardiac transcriptome revealed an RBM20-dependent regulation of alternative splicing. In addition to titin (TTN), we identified a set of 30 genes with conserved splicing regulation between humans and rats. This network is enriched for genes that have previously been linked to cardiomyopathy, ion homeostasis and sarcomere biology. Our studies emphasize the key role of post-transcriptional regulation in cardiac function and provide mechanistic insights into the pathogenesis of human heart failure.
              Article 0 comments Cited 230 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Johannes Backs: +49 6221 56-35271 , Johannes.backs@med.uni-heidelberg.de
                Journal
                Journal ID (nlm-ta): Basic Res Cardiol
                Journal ID (iso-abbrev): Basic Res. Cardiol
                Title: Basic Research in Cardiology
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 0300-8428
                ISSN (Electronic): 1435-1803
                Publication date (Electronic): 15 June 2018
                Publication date PMC-release: 15 June 2018
                Publication date (Print): 2018
                Volume: 113
                Issue: 4
                Electronic Location Identifier: 29
                Affiliations
                [1 ]ISNI 0000 0001 0328 4908, GRID grid.5253.1, Department for Molecular Cardiology and Epigenetics, , University Hospital Heidelberg, ; Im Neuenheimer Feld 669, 69120 Heidelberg, Germany
                [2 ]ISNI 0000 0001 0328 4908, GRID grid.5253.1, Department for Cardiology, Angiology and Pneumology, , University Hospital Heidelberg, ; Heidelberg, Germany
                [3 ]DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Heidelberg, Germany
                Article
                Publisher ID: 688
                DOI: 10.1007/s00395-018-0688-8
                PMC ID: 6003982
                PubMed ID: 29905892
                SO-VID: 4b941b42-1fa7-4473-9d2c-f6c0473e74bc
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 28 March 2018
                Date accepted : 11 June 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;
                Award ID: SFB 1118
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100010447, Deutsches Zentrum für Herz-Kreislaufforschung;
                Funded by: FundRef http://dx.doi.org/10.13039/501100002347, Bundesministerium für Bildung und Forschung;
                Categories
                Subject: Invited Review
                Custom metadata
                issue-copyright-statement © Springer-Verlag GmbH Germany, part of Springer Nature 2018

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: calcium,calmodulin,camkii,cardiomyocyte,inflammation,apoptosis
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: calcium, calmodulin, camkii, cardiomyocyte, inflammation, apoptosis

                Comments

                Comment on this article

                scite_

                Similar content332

                See all similar

                Cited by58

                See all cited by

                Most referenced authors1,764

                See all reference authors