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Fibrosis is similar to the process of scarring, in that both involve stimulated fibroblasts laying down connective tissue, including collagen and glycosaminoglycans.The process is initiated when immune cells such as macrophages release soluble factors that stimulate fibroblasts.
Fibroblasts can also migrate slowly over substratum as individual cells, again in contrast to epithelial cells. While epithelial cells form the lining of body structures, fibroblasts and related connective tissues sculpt the "bulk" of an organism. The life span of a fibroblast, as measured in chick embryos, is 57 ± 3 days. [4]
Dermal fibroblasts are cells within the dermis layer of skin which are responsible for generating connective tissue and allowing the skin to recover from injury. [1] Using organelles (particularly the rough endoplasmic reticulum), dermal fibroblasts generate and maintain the connective tissue which unites separate cell layers. [2]
It is a type of chronic pulmonary fibrosis characterized by a progressive and irreversible decline in lung function. [6] [3] [4] The tissue in the lungs becomes thick and stiff, which affects the tissue that surrounds the air sacs in the lungs. [7] Symptoms typically include gradual onset of shortness of breath and a dry cough. [1]
Pulmonary fibrosis is a condition in which the lungs become scarred over time. [1] Symptoms include shortness of breath, a dry cough, feeling tired, weight loss, and nail clubbing. [1] Complications may include pulmonary hypertension, respiratory failure, pneumothorax, and lung cancer. [2]
Myofibroblasts upregulate the expression of fibronectin, collagens, and hyaluronic acid during and after their differentiation from fibroblasts. Among these, the EDA isoform of fibronectin (EDA-FN), and collagen type I ( COL1A1 / COL1A2 ) are typical markers of myofibroblast-dependent synthesis of pro-fibrotic extracellular matrix.
Cardiac fibrosis commonly refers to the excess deposition of extracellular matrix in the cardiac muscle, but the term may also refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts. [1] Fibrotic cardiac muscle is stiffer and less compliant and is seen in the progression to heart failure.
Crowded between the collagen fibers are rows of fibroblasts, fiber-forming cells, that generate the fibers. Dense connective tissue forms strong, rope-like structures such as tendons and ligaments. Tendons attach skeletal muscles to bones; ligaments connect bones to bones at joints.