The body is an extremely complex mechanism and requires a precise balancing in order to function properly. Its processes are governed by a systematic interplay of factors, and recent studies have emphasised the importance of an enzyme, referred to as, CaM 11. This enzyme ensures that cardiac-muscles remain flexible and that muscle cells are sufficiently relaxed to operate effectively.
However, research conducted by Dr Wolgang Linke at the Institute of Physiology at Ruhr University, has found that blood-flow can actually be compromised by overactive CaM 11 enzymes, and feels that the effects of a body protein known as titin, could also play an important role in determining the strength and flexibility of cardiac muscles.
Titin is the most prevalent protein in the human-body and acts like a spring – either restricting or extending the movement of a muscle-cell. When it interacts with phosphate groups, a process is produced, known as phosphorylation – which relaxes cells further.
Within the studies, the researchers used the heart cells of regular mice, mice that had no CaM 11 enzymes and mice that over-produced the enzyme. In cells without the enzyme, titin phosphorylation was reduced by more than 50% when compared to the normal cells. These findings help to illustrate the key role that CaM 11 fulfils in the interplay between phosphate groups and titin. The research also investigated two areas in which the most malleable aspects of the structure of titin are phosphorylated by the enzyme – which are known as the PEVK and N2Bus regions. These regions also contain several amino acids that are crucial to the body’s health and wellbeing.
In follow up studies – the research team demonstrated that a lack of or abnormal amount of CaM 11 enzymes impacts upon the flexibility of muscle-cells, with increased levels being common amongst cases of heart-failure and chronic heart-disease.
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