clinical studies have now demonstrated unequivocally that modulation of inflammation can forestall the clinical complications of atherosclerosis
including targeting pivotal inflammatory pathways such as the inflammasomes
manipulating adaptive immunity
the ensuing inflammatory response orchestrates the progression and outcome of the disease.
This study targeted a specific pro-inflammatory cytokine, IL-1β, which has been implicated in atherogenesis through decades of experimental work. CANTOS showed that administration of an anti-IL-1β antibody to patients who were cardiovascularly stable after a myocardial infarction and were being treated according to current guidelines (including with statins) reduced recurrent major adverse cardiovascular events. Subsequent clinical trials with colchicine, another anti-inflammatory agent, have likewise demonstrated clinical benef
Regular physical activity lowered circulating counts of mononuclear cells as well as their ability to produce pro-inflammatory cytokines232
also decreases the number of circulating leukocytes
lammatory processes fuelled by SMCs (part b), macrophages (part c) and neutrophils (part d). b |
SMCs exposed to modified lipids or pro-inflammatory cytokines then release chemoattractants, including C-C motif chemokine 2 (CCL2) and CCL5 (refs10,11), which promote the recruitment of monocytes12 (Fig. 1a).
highly inflammatory milieu evokes a healing response
SMC transition to macrophage-like cells is likely pro-inflammatory and contributes to plaque vulnerability,
SMCs can also transition to fibroblast cells, which have previously been thought to have the opposite effects.
This transition depends on the transcription factor TCF21,
Single-cell RNA sequencing analyses
anti-TNF therapy has not engendered enthusiasm in patients at risk for heart failure, including those with coronary artery disease after ACS.
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