Pattern of organ remodeling in chronic non-communicable diseases is due to endogenous regulations and falls under the category of Kauffman’s self-organization: A case of arterial neointimal pathology

• Published in: Medical hypotheses 2020-10, Vol.143, p.110106-110106, Article 110106
• Main Author: Subbotin, Vladimir M.
• Format: Article
• Language: English
• Subjects: Accidental Falls; Arteries; Chronic diseases; Humans; Hyperplasia; Kauffman’s self-organization; Neointima; Neointimal formation; Noncommunicable Diseases; Pattern of organ remodeling; Unifying hypothesis
• ISSN: 0306-9877; 1532-2777
• DOI: 10.1016/j.mehy.2020.110106

Clinical diagnosis is based on analysis of pathologic findings that may result in perceived patterns. The same is true for diagnostic pathology: Pattern analysis is a foundation of the histopathology-based diagnostic system and, in conjunction with clinical and laboratory findings, forms a basis for the classification of diseases. Any histopathology diagnosis is based on the explicit assumption that the same diseased condition should result in formation of the same (or highly similar) morphologic patterns in different individuals; it is a standard approach in microscopic pathology, including that of non-communicable chronic diseases with organ remodeling. During fifty years of examining diseased tissues under microscopy, I keep asking the same question: Why is a similarity of patterns expected for chronic organ remodeling? For infection diseases, xenobiotic toxicity and deficiencies forming an identical pathologic pattern in different individuals is understandable and logical: The same infection, xenobiotic, or deficiency strikes the same target, which results in identical pathology. The same is true for Mendelian diseases: The same mutations lead to the same altered gene expressions and the same pathologic pattern. But why does this regularity hold true for chronic diseases with organ remodeling? Presumable causes (or risk factors) for a particular chronic disease differ in magnitude and duration between individuals, which should result in various series of transformations. Yet, mysteriously enough, pathological remodeling in a particular chronic disease always falls into a main dominating pattern, perpetuating and progressing in a similar fashion in different patients. Furthermore, some chronic diseases of different etiologies and dissimilar causes/risk factors manifest as identical or highly similar patterns of pathologic remodeling. I hypothesize that regulations governing a particular organ’s chronic remodeling were selected in evolution as the safest response to various insults and physiologic stress conditions. This hypothesis implies that regulations directing diseased chronic remodeling always preexist but normally are controlled; this control can be disrupted by a diverse range of non-specific signals, liberating the pathway for identical pathologic remodeling. This hypothesis was tested in an analysis of arterial neointimal formation, the identical pathology occurring in different diseases and pathological conditions: graft vascular disease in o