
Common ancestors: Chronic progressive diseases have the same pathogenesis
Author(s) -
Forrester James S.
Publication year - 2004
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960270403
Subject(s) - medicine , pathogenesis , disease , fibrosis , immunology , inflammation , homeostasis , bioinformatics , pathology , biology , endocrinology
In multiple organ systems, chronic progressive disease is characterized at the tissue level by increase in inflammatory cytokines, cell apoptosis and progressive fibrosis, suggesting a possible commonality of pathogenesis. This speculation is supported by the observation that elevated systemic levels of cytokines and/or CRP predict the appearance of disease, progression of disease, and disease complications. Some therapeutic interventions that reduce the expression of inflammatory cytokines, such as HMG Co-A reductase inhibitors, slow the progression of a number of chronic diseases, independent of their effect on cholesterol level. Taken together, these data suggest a unifying hypothesis for many chronic progressive diseases. Diverse noxious stimuli activate a normal protective inflammatory response. This response typically defervesces with elimination of the stimulus, reestablishing homeostasis. When homeostasis is not restored, that is, the inflammatory response persists, cell apoptosis and tissue fibrosis can result. The universality of this tissue response derives from the fact that all cells derive from the same blastocyst. Since cell differentiation results in different tissue functions, however, the clinical manifestations of disease are also vastly different, obscuring the underlying disease process. The relevance of this insight is that it provides a potential framework for testing old and new therapies which might inhibit a diverse set of clinical conditions at several levels of the disease process.