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Could Atherosclerosis Originate from Defective Smooth Muscle Cell Death (Apoptosis)?

Much recent research on the origin of atherosclerosis has concentrated on the role of growth factors and hormones in vascular smooth muscle growth. Overstimulation of vascular smooth muscle with growth factors or hormones is known to induce hyperplastic and/or hypertrophic responses in both cell and organ culture [1, 2]. The resulting increase in smooth muscle mass in these culture systems results from growth originating from many progenitor smooth muscle cells, i.e., a polyclonal response. This implication clearly contradicts the finding that atherosclerosis is a oligoclonal disorder. This result was most clearly demonstrated in 1973, in glucose-6-phosphate dehydrogenase (G6PD) heterozygous women [3, 4]. G6PD is present on the X chromosome and has two isoforms. Since one of the X chromosomes is randomly inactivated during development (Lyon hypothesis), G6PD heterozygous women are mosaics as regards to these two isoforms of G6PD. Normal arterial smooth muscle has numerous small regions (with a volume estimated of less than 0.1 mm3) that exhibit a single G6PD isoenzyme. Atherosclerotic plaques are typically composed of one to several larger regions (with a volume of 1 to 3 mm3) each exhibiting a single G6PD isoenzyme. This finding suggests that the smooth muscle cells in each of these regions originated from a single clone. After this finding was published, there was intense debate over whether atherosclerosis resulted from either hyperlipidemia [5] or clonal proliferation [6] . A search of the subsequent literature suggests that the hyperlipidemic hypothesis has been much more popular; a Medline search of "atherosclerosis" and "mosaicism" ("monoclonal" and "clonal" are not MESH headings) found only nine references between 1977 and 1993. I contend that we cannot