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Since the validation of the inflammatory paradigm in CANTOS and COLCOT, efforts to control the residual risk conferred by inflammation have centred on the NLRP3 inflammasome-driven IL-1\u03b2-IL6 axis. Interference with the co-stimulatory dyad CD40L\u2013CD40 and selective targeting of tumour necrosis factor-receptor associated factors (TRAFs), namely the TRAF6\u2013CD40 interaction in macrophages by small molecule inhibitors, harbour intriguing options to reduce established atherosclerosis and plaque instability without immune side effects. The chemokine system crucial for shaping immune cell recruitment and homoeostasis can be fine-tuned and modulated by its heterodimer interactome. Structure\u2013function analysis enabled the design of cyclic, helical, or linked peptides specifically targeting or mimicking these interactions to limit atherosclerosis or thrombosis by blunting myeloid recruitment, boosting regulatory T cells, inhibiting platelet activity, or specifically blocking the atypical chemokine MIF without notable side effects. Finally, adventitial neuroimmune cardiovascular interfaces in advanced atherosclerosis show robust restructuring of innervation from perivascular ganglia and employ sensory neurons of dorsal root ganglia to enter the central nervous system and to establish an atherosclerosis-brain circuit sensor, while sympathetic and vagal efferents project to the celiac ganglion to create an atherosclerosis-brain circuit effector. Disrupting this circuitry by surgical or chemical sympathectomy limited disease progression and enhanced plaque stability, opening exciting perspectives for selective and tailored intervention beyond anti-inflammatory strategies.<\/jats:p>","DOI":"10.1093\/eurheartj\/ehad304","type":"journal-article","created":{"date-parts":[[2023,5,20]],"date-time":"2023-05-20T20:00:45Z","timestamp":1684612845000},"page":"2672-2681","source":"Crossref","is-referenced-by-count":159,"title":["Novel mechanisms and therapeutic targets in atherosclerosis: inflammation and beyond"],"prefix":"10.1093","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4610-8714","authenticated-orcid":false,"given":"Christian","family":"Weber","sequence":"first","affiliation":[{"name":"Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universit\u00e4t M\u00fcnchen , Pettenkoferstra\u00dfe 9, 80336 M\u00fcnchen , Germany"},{"name":"German Centre for Cardiovascular Research (DZHK), partner site Munich Heart Alliance , Pettenkoferstra\u00dfe 9, 80336 M\u00fcnchen , Germany"},{"name":"Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre , Universiteitssingel 50, 6200 MD Maastricht , The Netherlands"},{"name":"Munich Cluster for Systems Neurology (SyNergy) , Munich , Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas J R","family":"Habenicht","sequence":"additional","affiliation":[{"name":"Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universit\u00e4t M\u00fcnchen , Pettenkoferstra\u00dfe 9, 80336 M\u00fcnchen , Germany"},{"name":"German Centre for Cardiovascular Research (DZHK), partner site Munich Heart Alliance , Pettenkoferstra\u00dfe 9, 80336 M\u00fcnchen , Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7474-9370","authenticated-orcid":false,"given":"Philipp","family":"von 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