Z-disc transcriptional coupling, sarcomeroptosis and mechanoptosis [corrected].
Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. Heart failure, which contributes significantly to the incidence and prevalence of cardiovascular-related diseases, can be the result of a myriad of diverse aetiologies including viral infections, coronary heart disease and genetic abnormalities--just to name a few. Interestingly, almost every type of heart failure is characterized by the loss of cardiac myocytes, either via necrosis, apoptosis or autophagy. While the former for a long time mainly has been characterized by passive loss of cells and only the latter two have been regarded as active processes, a new view is now emerging, whereby all three forms of cell death are regarded as different types of programmed cell death which can be induced via different stimuli and pathways, most of which are probably not well understood (Kung et al., Circulation Research 108(8):1017-1036, 2011). Here, we focus on the sarcomeric Z-disc, Z-disc transcriptional coupling and its role in pro-survival pathways as well as in striated muscle specific forms of cell death (sarcomeroptosis) and mechanically induced apoptosis or mechanoptosis.
Myocardial Genetics, British Heart Foundation-Centre of Research Excellence, National Heart & Lung Institute, Imperial College, Hammersmith Campus, London, UK. r.knoell@imperial.ac.uk
Ralph
R
Knöll
Byambajav
B
Buyandelger
D000818:Animals; D017209:Apoptosis; D001696:Biomechanical Phenomena; D009202:Cardiomyopathies / Q000378:metabolism / Q000473:pathology*; D064211:Connectin / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D009154:Mutation; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D025941:Protein Interaction Mapping; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D012518:Sarcomeres / Q000473:pathology*; D013312:Stress, Physiological; D014158:Transcription, Genetic; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
C491304:ANKRD1 protein, human; D064211:Connectin; D009124:Muscle Proteins; D009687:Nuclear Proteins; D012097:Repressor Proteins; C577292:TCAP protein, human; D016159:Tumor Suppressor Protein p53