Mast Cells: The Key Players in Cardiac Remodelling.
The term ‘Mast Cells’ originated from German term ‘Mastzellen’ that means fattened cells and were named because of large granules in their cytoplasm, which were expected to nourish the surrounding cells.
MCs were first characterized by Paul Ehrlich in 1878. The MCs originate from myeloid stem cells in bone marrow and the immature cells migrate to different tissues and later on develop into mature cells.
MCs are localized in organs rich in connective tissue and are abundantly present in skin, cardiovascular tissues, gastrointestinal tract, and
reproductive organs.
The degranulation of MCs does not cause their death and they are able to reconstitute their granules within few hours of degranulation by de novo synthesis.
The main biologically active degranulation products are histamine, serotonin, adenosine, heparin,
tryptase, chymase, cathepsin G, elastase, carboxy-peptidases and β-glucuronidase.
In addition, MCs have also been reported to release Tumor necrosis factor-α (TNF-α) and growth
factors like Transforming growth factor-β (TGF-β), nerve growth factor, vascular endothelial growth factor and fibroblast growth factor.
Cardiac remodelling is defined as change in size, shape and function of the heart due to changes at molecular and cellular level in response to hemodynamic load, neurohormonal activation and some other factors.
It composes various types of alterations including cardiac hypertrophy (concentric/eccentric),
dilatation and myopathy. The early events such as cardiac hypertrophy are protective in nature to tackle stress on heart, however, the chronic exposure to stress leads to mal-adaptations
such as dilatation and myopathy that consequently results in heart failure.
While MCs are reported to perform some physiological functions as mentioned earlier, the proliferation of cardiac MCs
and their recruitment from other organs has been reported in cardiac pathological conditions.
Pathol Lab Med Open J. 2016; 1(1): 7-10. doi: 10.17140/PLMOJ-1-103
