Targeting inflammation in atherosclerosis — from experimental insights to the clinic
By Oliver Soehnlein, Peter Libby. Nature reviews. Drug discovery, 2021
860 citations recorded by the source corpus.
Atherosclerosis, a dominant and growing cause of death and disability worldwide, involves inflammation from its inception to the emergence of complications. Targeting inflammatory pathways could therefore provide a promising new avenue to prevent and treat atherosclerosis. Indeed, clinical studies have now demonstrated unequivocally that modulation of inflammation can forestall the clinical complications of atherosclerosis. This progress pinpoints the need for preclinical investigations to refine strategies for combatting inflammation in the human disease. In this Review, we consider a gamut of attractive possibilities for modifying inflammation in atherosclerosis, including targeting pivotal inflammatory pathways such as the inflammasomes, inhibiting cytokines, manipulating adaptive immunity and promoting pro-resolution mechanisms. Along with lifestyle measures, pharmacological interventions to mute inflammation could complement traditional targets, such as lipids and hypertension, to make new inroads into the management of atherosclerotic risk. The contribution of inflammation to atherosclerosis is substantial, and is just beginning to be understood. In this Review, Soehnlein and Libby discuss how inflammation promotes atherosclerosis and its consequences, and how such processes could be targeted therapeutically. The potential pitfalls of targeting immune processes — namely the increased potential for infections — are also discussed, along with ways to modulate cardiovascular therapies in time and space to make them more effective.
Subfields: Epidemiology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6ee3ac62ee40729c7e96f07c783b13fe27418326
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Citations in the corpus
- Inflammation and atherosclerosis: signaling pathways and therapeutic intervention (2022, methodology): “Such determinants not only confer the appearance and functionality of macrophages but also define their heterogeneity at a single-cell level, suggesting that different subsets coexist within one tissue.(2) Given the key role of macrophages in atherosclerotic initiation, progression, and resolution, ”