The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
About this item
Full title
Author / Creator
Ucar, Ahmet , Gupta, Shashi K. , Fiedler, Jan , Erikci, Erdem , Kardasinski, Michal , Batkai, Sandor , Dangwal, Seema , Kumarswamy, Regalla , Bang, Claudia , Holzmann, Angelika , Remke, Janet , Caprio, Massimiliano , Jentzsch, Claudia , Engelhardt, Stefan , Geisendorf, Sabine , Glas, Carolina , Hofmann, Thomas G. , Nessling, Michelle , Richter, Karsten , Schiffer, Mario , Carrier, Lucie , Napp, L. Christian , Bauersachs, Johann , Chowdhury, Kamal and Thum, Thomas
Publisher
London: Nature Publishing Group UK
Journal title
Language
English
Formats
Publication information
Publisher
London: Nature Publishing Group UK
Subjects
More information
Scope and Contents
Contents
Pathological growth of cardiomyocytes (hypertrophy) is a major determinant for the development of heart failure, one of the leading medical causes of mortality worldwide. Here we show that the microRNA (miRNA)-212/132 family regulates cardiac hypertrophy and autophagy in cardiomyocytes. Hypertrophic stimuli upregulate cardiomyocyte expression of mi...
Alternative Titles
Full title
The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
Authors, Artists and Contributors
Author / Creator
Gupta, Shashi K.
Fiedler, Jan
Erikci, Erdem
Kardasinski, Michal
Batkai, Sandor
Dangwal, Seema
Kumarswamy, Regalla
Bang, Claudia
Holzmann, Angelika
Remke, Janet
Caprio, Massimiliano
Jentzsch, Claudia
Engelhardt, Stefan
Geisendorf, Sabine
Glas, Carolina
Hofmann, Thomas G.
Nessling, Michelle
Richter, Karsten
Schiffer, Mario
Carrier, Lucie
Napp, L. Christian
Bauersachs, Johann
Chowdhury, Kamal
Thum, Thomas
Identifiers
Primary Identifiers
Record Identifier
TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3657998
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3657998
Other Identifiers
ISSN
2041-1723
E-ISSN
2041-1723
DOI
10.1038/ncomms2090
