Na
. Arrhythmogenic cardiomyopathy (AC) is a heart muscle disease characterized by a progressive replacement of the ventricular myocardium with adipose and fibrous tissue. This disease is often associated with mutations in genes encoding desmosomal proteins in the majority of patients. Based on results...
Saved in:
Published in | Future cardiology Vol. 9; no. 4; pp. 467 - 470 |
---|---|
Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Future Medicine Ltd
01.07.2013
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | . Arrhythmogenic cardiomyopathy (AC) is a heart muscle disease characterized by a progressive replacement of the ventricular myocardium with adipose and fibrous tissue. This disease is often associated with mutations in genes encoding desmosomal proteins in the majority of patients. Based on results obtained from recent experimental models, a disturbed distribution of gap junction proteins and cardiac sodium channels may also be observed in AC phenotypes, secondary to desmosomal dysfunction. The study from Noorman et al. examined heart sections from patients diagnosed with AC and performed immunohistochemical analyses of N-cadherin, PKP2, PKG, Cx43 and the cardiac sodium channel Na
1.5. Altered expression/distribution of Cx43, PKG and Na
1.5 was found in most cases of patients with AC. The altered expression and/or distribution of Na
1.5 channels in AC hearts may play a mechanistic role in the arrhythmias leading to sudden cardiac death in AC patients. Thus, Na
1.5 should be considered as a supplemental element in the evaluation of risk stratification and management strategies. However, additional experiments are required to clearly understand the mechanisms leading to AC phenotypes. |
---|---|
AbstractList | . Arrhythmogenic cardiomyopathy (AC) is a heart muscle disease characterized by a progressive replacement of the ventricular myocardium with adipose and fibrous tissue. This disease is often associated with mutations in genes encoding desmosomal proteins in the majority of patients. Based on results obtained from recent experimental models, a disturbed distribution of gap junction proteins and cardiac sodium channels may also be observed in AC phenotypes, secondary to desmosomal dysfunction. The study from Noorman et al. examined heart sections from patients diagnosed with AC and performed immunohistochemical analyses of N-cadherin, PKP2, PKG, Cx43 and the cardiac sodium channel Na
1.5. Altered expression/distribution of Cx43, PKG and Na
1.5 was found in most cases of patients with AC. The altered expression and/or distribution of Na
1.5 channels in AC hearts may play a mechanistic role in the arrhythmias leading to sudden cardiac death in AC patients. Thus, Na
1.5 should be considered as a supplemental element in the evaluation of risk stratification and management strategies. However, additional experiments are required to clearly understand the mechanisms leading to AC phenotypes. |
Author | Shy, Diana Gillet, Ludovic Abriel, Hugues |
AuthorAffiliation | 1Department of Clinical Research, Ion Channel Research Group, University of Bern, Murtenstrasse 35, 3010 Bern, Switzerland 1Department of Clinical Research, Ion Channel Research Group, University of Bern, Murtenstrasse 35, 3010 Bern, Switzerland. hugues.abriel@dkf.unibe.ch |
AuthorAffiliation_xml | – name: 1Department of Clinical Research, Ion Channel Research Group, University of Bern, Murtenstrasse 35, 3010 Bern, Switzerland. hugues.abriel@dkf.unibe.ch – name: 1Department of Clinical Research, Ion Channel Research Group, University of Bern, Murtenstrasse 35, 3010 Bern, Switzerland |
Author_xml | – sequence: 1 givenname: Ludovic surname: Gillet fullname: Gillet, Ludovic – sequence: 2 givenname: Diana surname: Shy fullname: Shy, Diana – sequence: 3 givenname: Hugues surname: Abriel fullname: Abriel, Hugues |
BookMark | eNqdjcEKAiEURR_DBM1Uiz5E86mNuo6iVav2IvYEowyy-f8m6gtanXsWl9NDWx6FANYouJRoNikGjoor20CHRmtmpbPttLVxbBiMnUNf61UIZRy6DppTWMIshVul1Y8L2B72592RpfE1PqnGTCWS_9qdLjnmQh6F_wT9FPSovLLq398bkq82rg |
ContentType | Journal Article |
DOI | 10.2217/fca.13.38 |
DatabaseTitleList | |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
EISSN | 1744-8298 |
EndPage | 470 |
ExternalDocumentID | 10_2217_fca_13_38 |
GroupedDBID | - 0R 29H 3V. 4.4 53G 5GY 70G 7X7 88E 8AO 8FI 8FJ AAWTL ABUWG ACGFS ADBBV AFKRA AHMBA ALMA_UNASSIGNED_HOLDINGS BBAFP BENPR BPHCQ BVXVI CS3 EBS EHMNL F5P FYUFA H13 HZ IAO IEA IHR INH INR ITC M1P MV1 NTCAX O9- OVD P2P PQEST PQQKQ PQUKI PRINS PROAC PSQYO RFM |
ID | FETCH-futurescience_futuremedicine_10_2217_fca_13_383 |
ISSN | 1479-6678 |
IngestDate | Tue Jan 05 21:38:12 EST 2021 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 4 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-futurescience_futuremedicine_10_2217_fca_13_383 |
ParticipantIDs | futurescience_futuremedicine_10_2217_fca_13_38 |
ProviderPackageCode | NTCAX RFM 70G |
PublicationCentury | 2000 |
PublicationDate | 2013-July-01 |
PublicationDateYYYYMMDD | 2013-07-01 |
PublicationDate_xml | – month: 07 year: 2013 text: 2013-July-01 day: 01 |
PublicationDecade | 2010 |
PublicationTitle | Future cardiology |
PublicationYear | 2013 |
Publisher | Future Medicine Ltd |
Publisher_xml | – name: Future Medicine Ltd |
SSID | ssj0037919 |
Score | 3.8922987 |
Snippet | . Arrhythmogenic cardiomyopathy (AC) is a heart muscle disease characterized by a progressive replacement of the ventricular myocardium with adipose and... |
SourceID | futurescience |
SourceType | Publisher |
StartPage | 467 |
SubjectTerms | 1.5 arrhythmogenic cardiomyopathy connexin 43 immunohistochemistry intercalated disk Na |
Title | Na |
URI | http://dx.doi.org/10.2217/fca.13.38 |
Volume | 9 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnR1dS8Mw8JgbiCLiJ36zB19btyZpm8epm0NYEZmwt5K0qeylg7H64K_30rRdqz44X0Ib8nHkrvfV3B3AbcR6kjPZsxRnwqJRgt8ck4mFxOQh4FHi5z7dSeCO3-jzjM3WNTPz6JKVtKPPX-NK_oNV7EO86ijZDTBbLYod-Iz4xRYxjO2fcByIum45ytOD6FzT8bzhLH_S8X7GAs_ixcc8qtwq5ogfkUQq7jyQaDybDNfZe6YabgFdosGruwWKLSfFD_raHSHN5ajHLdc1tXNsZfo8Si3fMSWhS9bIaxRAa2yOmhIahcSkpvTHd2bsOHkGpyQSdp_YxF9LnOoeIFogelSIY8I-CYm_BR3H4wyt6M79MHh5LYUq8Xheo6WC3CSJ0pPvqg12Yc8kYmkoD7miMD2A_ULD7w4Mug6hpdIj2C6P6BhagTgBNhpOH8ZWY6HQvJW3HcIfYJNTaKeLVJ1Bl1M_lo6vHJWg4O9JkaBBR2ImXKETDZFzsDdb-2LTCZewsyaIK2ivlpm6Rs1pJW-KU_0Csx8eYw |
link.rule.ids | 315,786,790,27957,27958 |
linkProvider | ProQuest |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Na&rft.jtitle=Future+cardiology&rft.au=Gillet%2C+Ludovic&rft.au=Shy%2C+Diana&rft.au=Abriel%2C+Hugues&rft.date=2013-07-01&rft.pub=Future+Medicine+Ltd&rft.issn=1479-6678&rft.eissn=1744-8298&rft.volume=9&rft.issue=4&rft.spage=467&rft.epage=470&rft_id=info:doi/10.2217%2Ffca.13.38&rft.externalDocID=10_2217_fca_13_38 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1479-6678&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1479-6678&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1479-6678&client=summon |