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Maturation of the heart
1Department of Pediatrics, Baylor College of Medicine, Houston, Texas.
Insights
Heart function improves from fetus to adult due to increased contractile proteins and altered ion pump activity. Molecular changes, especially in myosin, drive this perinatal maturation, though not fully explaining it in larger species.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Developmental Biology
Background:
- Myocardial contractile function progressively increases from fetal to adult stages.
- The perinatal period involves significant maturation of heart muscle function.
Purpose of the Study:
- To review biochemical and molecular mechanisms regulating perinatal heart function maturation.
- To highlight new findings on the regulation of cardiac contraction during development.
Main Methods:
- Review of existing literature on myocardial development.
- Analysis of biochemical and molecular processes in cardiac cells.
- Comparison of fetal, newborn, and adult cardiac function.
Main Results:
- Cardiac development increases sarcoplasmic reticulum and myofibril quantity.
- Ion pump protein function is lower in fetuses/newborns than adults.
- Myosin isoform shifts significantly contribute to enhanced contractility in some species (e.g., rats).
Conclusions:
- Perinatal heart maturation involves increased cellular organelles and altered ion handling.
- Molecular regulation, particularly myosin isoform changes, is key for myofibrillar function.
- Current molecular understanding may not fully explain maturation in all species, especially larger ones.
Abstract:
The transition from fetal to newborn to adult previously has been associated with a progressive increase in myocardial contractile function. The purpose of this review is to summarize new information on the biochemical and molecular processes that regulate the perinatal maturation of heart function. The developing heart experiences a perinatal increase in the cellular quantity of the sarcoplasmic reticulum and the myofibrils, the organelles that regulate and utilize cytosolic calcium to produce cardiac contraction. It also has become evident that the function of the available ion pump proteins is reduced in fetuses and newborns compared to adults of the same species. The resultant limited regulation of cytosolic calcium concentrations by the sarcoplasmic reticulum enhances the role of the sarcolemma in this process. Although it appears that the perinatal maturation of sarcoplasmic reticular function is not under direct molecular regulation, alternative splicing may regulate its gene products. A great deal of the perinatal maturation of myofibrillar protein function appears to be regulated by molecular processes. This has been best demonstrated in detail for myosin. In some species, such as the rat, much of the perinatal increase in myocardial contractile function can be explained by a parallel change in myosin isoforms. This isoform shift alters the activity of its ion pump, thereby allowing it to utilize more calcium. In contrast, the perinatal maturation of contractile function in several larger species cannot be explained fully by the extent of the molecular changes that have been identified currently in these species.