Abstract
Alterations in fibrinogen metabolism frequently occur in physiologic adaptations to stress and also accompany many pathologic states. Unfortunately, the significance of such alterations remains unknown. However, fibrin deposits can impair organ function and are likely to be major contributors to the debilitation eventuating with numerous diseases of unrelated etiologies. Fibrin deposition and its removal are recognized problems in the thrombotic diseases such as myocardial infarction and cerebrovascular thrombosis. But only recently has fibrin deposition alone and in association with immunologic diseases been considered of consequence in renal dysfunction [1]. Even more recent is the still limited appreciation of the role of fibrin deposits in perpetuating and recycling joint inflammations occuring in rheumatoid diseases [2, 3]. Of obvious value is the further identification and improved understanding of the mechanisms available for resolving the problems of fibrinogen metabolism and fibrin deposition and degradation. The purpose of this communication is to report on the cellular mechanisms for eliminating altered fibrinogen and fibrin and their degradation products from the circulation.
Supported by research grant HE 04712 of the National Institutes of Health, U.S. Public Health Service and the Michigan Heart Association.
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Barnhart, M.I., Cress, D.C. (1967). Plasma Clearance of Products of Fibrinolysis. In: Luzio, N.R.D., Paoletti, R. (eds) The Reticuloendothelial System and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7796-2_44
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DOI: https://doi.org/10.1007/978-1-4684-7796-2_44
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