MECHANICAL LOAD AND POLYPEPTIDE GROWTH-FACTORS STIMULATE CARDIAC FIBROBLAST ACTIVITY
MECHANICAL LOAD AND POLYPEPTIDE GROWTH-FACTORS STIMULATE CARDIAC FIBROBLAST ACTIVITY
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DOI：
10.1111/j.1749-6632.1995.tb17446.x
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发表时间：
1995-01-01
期刊：
影响因子：
--
通讯作者：
BISHOP, JE
中科院分区：
文献类型：
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作者：
BUTT, RP;LAURENT, GJ;BISHOP, JE
胶原纤维在心肌中形成一个由编织和支柱组成的网络，将肌细胞和毛细血管相互连接，防止相邻肌肉纤维在心脏周期中滑动，协调力量的传递，并在收缩期间保持毛细血管通畅。1心脏胶原主要是由心脏成纤维细胞产生的I型和III型纤维胶原。2‘3型，IV，V，VI和VIII型也被鉴定出来，但不到心肌总胶原含量的10%。在心肌肥厚的发展过程中，胶原沉积增加，这可能导致心肌纤维化，特别是当肥厚是由于压力超负荷所致的时候。4-7过量的胶原蛋白通过增加心脏僵硬来损害心脏的舒张期功能。8 I型胶原的相对比例(与I型和III型相比)也可能增加，5-6，9可能进一步促进心脏的舒张期僵硬，这是由于I型胶原纤维的抗张强度更大。
Collagen fibers form a network of weaves and struts in the myocardium that interconnect myocytes and capillaries, preventing slippage of adjacent muscle fibers during the cardiac cycle, coordinating the delivery of force and maintaining capillary patency during contraction. 1 Cardiac collagens are principally the type I and III fibrillar collagens, produced by cardiac fibroblasts. 2'3 Types IV, V, VI and VIII have also been identified but represent less than 10% of the total cardiac collagen content.During the development of cardiac hypertrophy there is an increase in collagen deposition which may lead to cardiac fibrosis, particularly if the hypertrophy is due to pressure overload. 4-7 Excess collagen impairs the diastolic function of the heart by increasing cardiac stiffness. 8 The relative proportion of type I collagen (compared to types I and III) may also increase, 5-6, 9 possibly contributing further to the diastolic stiffness of the heart, due to the greater tensile strength of the type I collagen fibers.