Progress of NLRP3 inflammasome in the pathogenesis of heart disease

doi:10.16352/j.issn.1001-6325.2023.07.1162

Abstract

Abstract: NLRP3 inflammatsome is the most characteristic inflammasome. It can play some roles in the pathogenesis of heart diseases such as heart failure, myocardial infarction, atherosclerosis and arrhythmia. Inhibiting the activation of NLRP3 inflammasome can effectively treat heart diseases. The assembly and activation process of inflammasome are complex. Revealing its activation process and its relationship with heart disease may develop new drugs targeting at the prevention and treatment of heart disease.

Key words: NLRP3 inflammasome, cardiovascular disease, inflammatory reaction

CLC Number:

R392.12

GAO Yuan, ZHENG Gang, QI Jing, ZHANG Feng. Progress of NLRP3 inflammasome in the pathogenesis of heart disease[J]. Basic & Clinical Medicine, 2023, 43(7): 1162-1166.

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URL: http://journal11.magtechjournal.com/Jwk_jcyxylc/EN/10.16352/j.issn.1001-6325.2023.07.1162

http://journal11.magtechjournal.com/Jwk_jcyxylc/EN/Y2023/V43/I7/1162

References

[1] Schunk S,Kleber M,März W, et al. Genetically determined NLRP3 inflammasome activation associates with systemic inflammation and cardiovascular mortality[J].Eur Heart J, 2021, 42: 1742-1756.
[2] Hoseini Z,Sepahvand F,Rashidi B, et al. NLRP3 inflammasome: its regulation and involvement in atherosclerosis[J].J Cell Physiol, 2018, 233: 2116-2132.
[3] Pellegrini C,Martelli A,Antonioli L, et al. NLRP3 inflammasome in cardiovascular diseases: pathophysiological and pharmacological implications[J].Med Res Rev, 2021, 41: 1890-1926.
[4] Corcoran S,Halai R,Cooper M, et al. Pharmacological inhibition of the nod-like receptor family pyrin domain containing 3 inflammasome with MCC950[J].Pharmacol Rev, 2021, 73: 968-1000.
[5] Wang ZH,Wei K,Lu C, et al. Targeting NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome in cardiovascular disorders[J].Arterioscler Thromb Vasc Biol, 2018, 38: 2765-2779.
[6] Christgen S,Place D,Kanneganti T.Toward targeting inflammasomes: insights into their regulation and activation[J].Cell Res, 2020, 30: 315-327.
[7] Liu DL,Zeng X,Li X, et al. Role of NLRP3 inflamma-some in the pathogenesis of cardiovascular diseases[J].Basic Res Cardiol, 2018, 113: 265-273.
[8] Chong WC,Shastri M,Peterson G, et al. The complex interplay between endoplasmic reticulum stress and the NLRP3 inflammasome: a potential therapeutic target for inflammatory disorders[J].Clin Transl Immunol, 2021, 10: 381-389.
[9] Shen J,Ma H,Wang C.Triptolide improves myocardial fibrosis in rats through inhibition of nuclear factor kappa B and NLR family pyrin domain containing 3 inflammasome pathway[J].Korean J Physiol Pharmacol, 2021, 25: 533-543.
[10] Abbate A,Toldo S,Marchetti C, et al. Interleukin-1 and the inflammasome as therapeutic targets in cardiovascular disease[J].Circ Res, 2020, 126: 1260-1280.
[11] Lim G.Heart failure: clonal haematopoiesis, IL-1β, and the NLRP3 inflammasome in HF[J].Nat Rev Cardiol, 2018, 15: 198-212.
[12] Sano S,Oshima K,Wang Y, et al. Tet2-Mediated clonal hematopoiesis accelerates heart failure through a mechanism involving the IL-1β/NLRP3 inflammasome[J].J Am Coll Cardiol, 2018, 71: 875-886.
[13] Ridker P,Rane M.Interleukin-6 signaling and anti-interleukin-6 therapeutics in cardiovascular disease[J].Circ Res, 2021, 128: 1728-1746.
[14] Grebe A,Hoss F,Latz E.NLRP3 inflammasome and the IL-1 pathway in atherosclerosis[J].Circ Res, 2018, 122: 1722-1740.
[15] Fuster J.Integrated stress response inhibition in atherosclerosis: preventing the stressed-out plaque[J].J Am Coll Cardiol, 2019, 73: 1170-1172.
[16] Chen X,Guo X,Ge Q, et al. ER stress activates the NLRP3 inflammasome: a novel mechanism of atherosclerosis[J].Oxid Med Cell Longev, 2019, 2019: 346-362.
[17] Abbate A,Toldo S,Marchetti C, et al. Interleukin-1 and the inflammasome as therapeutic targets in cardiovascular disease[J].Circ Res, 2020, 126: 1260-1280.
[18] Sreejit G,Abdel LA,Athmanathan B, et al. Neutrophil-derived S100A8/A9 amplify granulopoiesis after myo-cardial infarction[J].Circulation, 2020, 141: 1080-1094.
[19] Everett B,Mac FG,Thuren T, et al. Inhibition of interleukin-1β and reduction in atherothrombotic cardiovascular events in the CANTOS trial[J].J Am Coll Cardiol, 2020, 76: 1660-1670.
[20] Lv SL,Zeng ZF,Gan WQ, et al. Lp-PLA2 inhibition prevents Ang Ⅱ-induced cardiac inflammation and fibrosis by blocking macrophage NLRP3 inflammasome activation[J].Acta Pharmacol Sin, 2021, 42: 2016-2032.
[21] Yan Z,Qi Z,Yang X, et al. The NLRP3 inflammasome: multiple activation pathways and its role in primary cells during ventricular remodeling[J].J Cell Physiol, 2021, 236: 5547-5563.
[22] Scott L,Fender A,Saljic A, et al. NLRP3 inflammasome is a key driver of obesity-induced atrial arrhythmias[J].Cardiovasc Res, 2021, 117: 1746-1759.
[23] Wei Z,Fei Y,Wang Q, et al. Loss of Camk2n1 aggravates cardiac remodeling and malignant ventricular arrhythmia after myocardial infarction in mice via NLRP3 inflammasome activation[J].Free Radic Biol Med, 2021, 167: 243-257.