**14. Relationship between lipidosis and other atherosclerotic manifestations**

Blood serum and LDL isolated from blood of atherosclerotic patients capable to induce intracellular lipid accumulation can also lead to other atherogenic manifestations in cultured cells of subendothelial human intima [91]. Preincubation of cells with atherogenic serum or LDL, causing intracellular lipid accumulation, also stimulates cell proliferation and synthesis of collagen, glycosaminoglycans, and total protein [91, 93]. Thus, blood serum and LDL of atherosclerotic patients have a broad spectrum of atherogenic properties, causing all main manifestations of atherosclerosis: enhancement of cell proliferation, fibrosis, and lipidosis. Direct contact of modified LDL with cells is not necessary for stimulation of proliferation and production of the connective tissue matrix components. Increased proliferative activity and extracellular matrix production are preserved for several days after removal of atherogenic LDL from the culture medium [91]. This finding suggests that not the interaction between LDL and cells but rather the consequences of this interaction, i.e., lipid accumulation, which coincides with increased cell proliferation and extracellular matrix production, are the crucial aspect in the realization of atherogenic potential at the cellular level.

As mentioned above, lipid accumulation affects the integrity of cellular network in human aortic intima. In the lipid-rich lesions, where the content of lipid-laden and foam cells is high, rupture of the network have been observed. It should be noted that cells not contacting with their neighbors are often overladen with lipids [67].

A decrease in the rate of intracellular communication between cultured cells caused by modified LDL which induce intracellular lipid accumulation may account for the decreasing of cell contacts and their disruption. In fact, incubation of subendothelial intimal cells with modified LDL results in accumulation of intracellular lipids with a parallel reduction of the degree of intercellular communication [73]. It is reasonable to suggest that the reduction of cell‐ to-cell contacts is a consequence of lipid accumulation.
