Tissue fibrosis: a principal evidence for the central role of Misrepairs in aging

Tissue fibrosis is the phenomenon that a tissue has progressive deposition of excessive collagen fibers with age. Tissue fibrosis is a typical aging change, and it is the main cause for diseases such as essential arterial hypertension, benign prostatic hyperplasia and senile chronic bronchitis/emphysema. Fibrosis is known to be a result of repairs of a tissue with collagen fibers. In our Misrepair-accumulation aging theory, we proposed a generalized concept of Misrepair, which is defined as incorrect reconstruction of an injured living structure. Thus a repair with collagen fibers for replacing dead cells or injured extracellular matrixes is a kind of Misrepair. Progressive process of fibrosis in an organism demonstrates that: A. a process of Misrepair exists; B. Misrepairs are unavoidable; and C. Misrepairs accumulate. Thus, the phenomenon of fibrosis is a principle evidence for demonstrating the central role of Misrepair in aging. Accumulation of collagen fibers in a tissue is focalized and inhomogeneous, resulting in the development of bands of hyaline degeneration. In arteriosclerotic hypertension and in chronic bronchitis/emphysema, the deposed collagen fibers in arterial walls and airway walls are used for replacing the broken elastic fibers and myofibers, which are injured during repeated deformations of the walls. Stiffness of arterial walls promotes enlargement of myofibers, leading to thickness of the walls. In Benign prostatic hyperplasia, the deposed collagen fibers in muscular tissues are used for replacing broken myofibers, which are injured during ejaculations. Muscular fibrosis results in accumulation of prostatic fluid and expansion of the prostate. Apart from these diseases, scar formation and wrinkle formation are a part of fibrosis of the skin, and senile hair-loss and hair-whitening are results of dermal fibrosis.