English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Necrotic and apoptotic cell deaths are the two main causes of the heart's loss of cardiac tissue and haemodynamic function after myocardial infarction (MI). The loss of functional cardiac myocytes through necrotic/apoptotic processes during ischaemia in the absence of de novo cell proliferation has been postulated to be a fundamental cause of ventricular remodelling, increased tissue fibrosis, and diminished ventricular pump function.In the past decade, several approaches have been tested hoping to increase the number of myocytes after MI, including transplantation of progenitor or adult cells,1 mobilization of endogenous stem cells,2 and cell cycle activation.3 Each of these approaches demonstrated some degree of myocardial functional improvement, with cell cycle activation being the most promising one.3Although there is evidence for adult cardiomyocyte proliferation,4 it is clear that this process is not capable of fully recovering the … *Corresponding author. Tel: +55 41 3316 3230/3237; fax: +55 41 3316 3267. E-mail address : adcosta{at}tecpar.br; adtcosta{at}gmail.com

Divide to survive: myocardial regeneration and functional recovery after cell cycle activation in injured hearts