Atherosclerosis

Running head: ATHEROSCLEROSIS 1
Atherosclerosis
Name
Institution

ATHEROSCLEROSIS 2
Atherosclerosis
Ideally, atherosclerosis is considered to be an inflammatory illness that often results from
high plasma concentrations of cholesterol. In most cases, atherosclerosis is regarded to be a focal
disease procedure that happens primarily at sites of disturbed laminar flow. Notably, such sites
include the arterial branch sections as well as bifurcations. Various morphological studies of the
Atherosclerosis have indicated that the main initiating steps are the overall sub-endothelial
accruals of the Apo lipoprotein B that contain lipoproteins. Essentially, this protein has been
presumed to be one of the risk factors for atherosclerosis in the human body. Even though people
have tried to change their lifestyle particularly concerning diet with the aim of lowering the
overall concentration of cholesterol in plasma, cardiovascular illness remains the primary cause
of deaths in the USA, Europe, as well Asian countries. In this light, the abrasion of
atherosclerosis characterizes a series of specific molecular as well as cellular responses that can
be described as an inflammatory disease. This paper proposes to discuss the subsequent pertinent
experimental and patient-based studies that have validated the proposition of Russell Ross
regarding atherosclerosis.
Various studies and pathophysiological observations have been done regarding human as
well as animals leading to the overall formulation of the response to the injury hypothesis that
was made concerning atherosclerosis (Ross, 1999). Notably, this was done as initially proposed
that endothelial happened to be the first step in atherosclerosis. Researches show that the
endothelial dysfunction resulting from injuries often leads to compensatory responses that are
responsible for altering the natural homeostatic properties of the endothelium (Clarkson, 2018).
Injuries have as well been tipped to induce the overall endothelium to contain procoagulant
rather than anticoagulant thus forming a vasoactive molecule, growth factor, and cytokines. In

ATHEROSCLEROSIS 3
case the inflammatory response fails to neutralize or even remove the offending agents, it is
presumed to continue indefinitely. If these responses continue without being abated, they tend to
thicken the entire walls of the artery which is then compensated by an apparent dilation so that
the lumen appears to be unaltered.
Furthermore, continual inflammatory in a patient may result in an apparent increase in the
overall numbers of macrophages as well as lymphocytes. Both of these elements tend to emigrate
from the blood thus multiplying within the lesion (Clarkson, 2018). Research indicates that the
activation of the aid cells can lead to the release of hydrolytic enzymes, growth factor, cytokines,
and chemokine. This can induce more damages leading to focal necrosis. Therefore,
accumulation of various mononuclear cells, proliferation, and migration of smooth muscle cells
leading to the formation of fibrous tissue cells (Childs et al., 2016). This leads to the enlargement
as well as the restructuring of the entire lesion making it be covered with fibrous caps overlying
core of the lipid and the necrotic tissues (Ross, 1999). The artery may fail to compensate by
dilation at some point; at this point, the lesion may tend to intrude into the lumen and thus
altering the overall flow of blood in an individual body.
There have been various experiments that have been done to justify the assertions made
by Russell Ross regarding atherosclerosis in patients. One modification is the
Hypercholesterolemia and Modified Lipids and Lipoproteins. This is the overall modification of
the LDL through oxidation. Glycation especially in diabetes, as well as aggression, incorporation
into the complexes of the immune system is regarded to be the leading cause of injury on the
endothelium. In case the LDL in a patient’s body is trapped in a particular artery, they may tend
to undergo the process of oxidation thus being internalized by the macrophages through the
scavenger receptors on the surface of the respective cells (Ross, 1999). The overall