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Endothelial dysfunction may be involved in the development of atherosclerosis [5] [6] [7] and may predate vascular pathology. [5] [8] Endothelial dysfunction may also lead to increased adherence of monocytes and macrophages, as well as promoting infiltration of low-density lipoprotein (LDL) in the vessel wall. [9]
The chronic endothelial injury hypothesis is one of two major mechanisms postulated to explain the underlying cause of atherosclerosis and coronary heart disease (CHD), the other being the lipid hypothesis. Although an ongoing debate involving connection between dietary lipids and CHD sometimes portrays the two hypotheses as being opposed, they ...
Blood vessel damage from insulin spikes. Insulin acts on many different cell types in the body, including muscle cells, adipose (fatty) tissue, liver, brain, and endothelial cells lining the blood ...
The endothelium (pl.: endothelia) is a single layer of squamous endothelial cells that line the interior surface of blood vessels and lymphatic vessels. [1] The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.
The mechanism by which AGEs induce damage is through a process called cross-linking that causes intracellular damage and apoptosis. [18] They form photosensitizers in the crystalline lens, [19] which has implications for cataract development. [20] Reduced muscle function is also associated with AGEs. [21]
While short-term inflammation is a natural and necessary part of the body’s healing process, prolonged inflammation (aka chronic inflammation) can contribute to the onset of chronic conditions ...
Diminished supply of nitric oxide can lead to vascular damage, such as endothelial dysfunction and vascular inflammation. Vascular damage can lead to decreased blood flow to the extremities, causing the diabetic patient to be more likely to develop neuropathy and non-healing ulcers, and to be at a greater risk for lower limb amputation.
Urinary water loss, when the body water homeostat is intact, is a compensatory water loss, correcting any water excess in the body. However, since the kidneys cannot generate water, the thirst reflex is the all-important second effector mechanism of the body water homeostat, correcting any water deficit in the body.