Molecular aspects of cardiac hypertrophy.
Despite continuous interest in cardiac hypertrophy, our knowledge of its molecular aspects is still elementary. Recently, however, several advancements of particular interest have been made: (a) Nuclei of muscle and nonmuscle cells have been separated, allowing for the first time the study of nuclear activity in specified cells (18). (b) Cardiac growth induced by pressure-overload (72) or by hormone treatment (26) has been shown to lead to myosin of altered ATPase, and strong evidence suggests that new species of myosin molecules thus appear. (c) The basis for assessment of protein synthesis and degradation has been established (46, 48). (d) Methods are being developed to supplement radioautography in evaluating cell proliferation (42, 59, 69). (e) In spontaneously hypertensive rats it has been shown that blood pressure might not be the sole factor responsible for cardiac enlargement, but that hypertrophy can be the result of genetic cardiovascular abnormality (19, 66). (f) A hypothesis relating the extent of energy utilization to the nuclear activity via NAD+ metabolism has been proposed, which allows for experimental verification (43).
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D002455:Cell Division; D004247:DNA / Q000378:metabolism; D009124:Muscle Proteins / Q000378:metabolism; D009206:Myocardium / Q000166:cytology / Q000378:metabolism* / Q000648:ultrastructure; D009218:Myosins / Q000378:metabolism; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D014158:Transcription, Genetic
D009124:Muscle Proteins; D012333:RNA, Messenger; D004247:DNA; D000251:Adenosine Triphosphatases; D009218:Myosins