An update on the role of TRIM/NLRP3 signaling pathway in atherosclerosis - 26/02/23

Abstract |
Atherosclerosis (AS) is a chronic inflammatory disease of large and medium arteries that includes lipid metabolism disorder and recruitment of immune cells to the artery wall. An increasing number of studies have confirmed that inflammasome over-activation is associated with the onset and progression of atherosclerosis. The NLRP3 inflammasome, in particular, has been proven to increase the incidence rate of cardiovascular diseases (CVD) by promoting pro-inflammatory cytokine release and reducing plaque stability. The strict control of inflammasome and prevention of excessive inflammatory reactions have been the research focus of inflammatory diseases. Tripartite motif (TRIM) is a protein family with a conservative structure and rapid evolution. Several studies have demonstrated the TRIM family's regulatory role in mediating inflammation. This review aims to clarify the relationship between TRIMs and NLRP3 inflammasome and provide insights for future research and treatment discovery.
Il testo completo di questo articolo è disponibile in PDF.Graphical Abstract |
Highlights |
• | The molecular mechanisms of the NLRP3 inflammasome in atherosclerosis. |
• | The novel drug therapy and gene editing therapies targeting the NLRP3 inflammasome in atherosclerosis. |
• | The signaling pathways of the TRIM family interact with the NLRP3 inflammasome. |
• | The potential atherosclerosis therapies targeting TRIM/NLRP3 inflammasome axis. |
Keywords : Atherosclerosis, NLRP3 inflammasome, TRIM family
Mappa
Vol 160
Articolo 114321- aprile 2023 Ritorno al numeroBenvenuto su EM|consulte, il riferimento dei professionisti della salute.
L'accesso al testo integrale di questo articolo richiede un abbonamento.
Già abbonato a @@106933@@ rivista ?
