A tentative molecular-biological hypothesis for arteriosclerosis

Area of Science:

• Cardiovascular Science
• Aging Research
• Molecular Biology

Background:

• Arteriosclerosis complications are leading causes of mortality in industrialized nations.
• The prevailing lipid theory, focusing on cholesterol's detrimental effects, has limitations in explaining arteriosclerosis phenomena.
• Existing theories fail to account for cholesterol homeostasis, early atheroma composition, and lesion distribution/progression.

Purpose of the Study:

• To explore alternative etiological factors for arteriosclerosis beyond the lipid theory.
• To investigate the role of aging, autoimmune processes, and extrachromosomal genetic elements in arteriosclerosis.
• To re-evaluate the contribution of lipid changes as adaptive mechanisms.

Main Methods:

• This study presents a theoretical framework and literature review, not empirical data.
• Analysis of existing data on cholesterol metabolism, aging, and molecular biology.
• Integration of findings related to autoimmune responses and extrachromosomal organisms (viruses, plasmids, viroids).

Main Results:

• Arteriosclerosis is proposed as an integral part of normal aging, linked to molecular-biological changes.
• Autoimmune processes and extrachromosomal genetic elements (viruses, plasmids, viroids) are implicated in lesion development and clinical manifestation.
• Lipid changes are reinterpreted as adaptive responses to vessel damage caused by DNA alterations.

Conclusions:

• Arteriosclerosis etiology is multifactorial, involving aging, autoimmunity, and genetic elements, not solely cholesterol.
• Extrachromosomal organisms may explain lesion variability, location, and the programmed appearance of symptoms.
• Lipid alterations are likely secondary adaptive mechanisms rather than primary causes.