Autophagy Regulates Remodeling in Unloaded Heart

Rajabi, Mitra; Salazar, Rebecca; Razeghi, Peter; Stepkowski, Stanislaw M.; Taegtmeyer, Heinrich

doi:10.1016/j.cardfail.2007.06.388

Cited by 1 publication

(1 citation statement)

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“…We found that markers of autophagy including LC3, Atg5, and Agt12 are increased at both the RNA and protein levels in the unloaded heart. 112 In contrast, the failing human heart already expresses elevated levels of autophagy markers but when implanted with an LVAD, autophagy markers are downregulated. 68,69 These data suggest that autophagy could be an adaptive mechanism in the failing heart; however, they do not rule out the possibility that autophagy in end-stage heart failure could be maladaptive.…”

Section: Pathways Of Protein Turnovermentioning

confidence: 99%

Taking pressure off the heart: the ins and outs of atrophic remodelling

Baskin

Taegtmeyer

2011

Cardiovascular Research

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Our work on atrophic remodelling of the heart has led us to appreciate the simple principles in biology: (i) the dynamic nature of intracellular protein turnover, (ii) the return to the foetal gene programme when the heart remodels, and (iii) the adaptive changes of cardiac metabolism. Although the molecular mechanisms of cardiac hypertrophy are many, much less is known regarding the molecular mechanisms of cardiac atrophy. We state the case that knowing more about mechanisms of atrophic remodelling may provide insights into cellular consequences of metabolic and haemodynamic unloading of the stressed heart. Overall we strive to find an answer to the question: 'What makes the failing heart shrink and become stronger?' We speculate that signals arising from intermediary metabolism of energy-providing substrates are likely candidates.

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Section: Pathways Of Protein Turnovermentioning

confidence: 99%