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Nlrp3 Inflammasome Pathway in Atherosclerosis: Focusing on the Therapeutic Potential of Non-Coding Rnas Publisher Pubmed



Alhawary SIS1 ; Jasim SA2 ; Romeroparra RM3 ; Bustani GS4 ; Hjazi A5 ; Alghamdi MI6 ; Kareem AK7 ; Alwaily ER8 ; Zabibah RS9 ; Gupta J10 ; Mahmoudi R11 ; Hosseinifard S12
Authors
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Authors Affiliations
  1. 1. Department of Business Administration, Business School, Al al-Bayt University, P.O. BOX 130040, Mafraq, 25113, Jordan
  2. 2. Medical Laboratory Techniques Department, Al-maarif University College, Al-anbar-Ramadi, Iraq
  3. 3. Universidad Continental, Lima, Peru
  4. 4. College of Dentistry, The Islamic University, Najaf, Iraq
  5. 5. Department of Medical Laboratory Sciences, College of Applied Medical Sciences, Prince Sattam bin Abdulaziz University, Al-Kharj, 11942, Saudi Arabia
  6. 6. Al-Baha University, Al-Baha, Saudi Arabia
  7. 7. Biomedical Engineering Department, Al-Mustaqbal University College, Hillah, 51001, Iraq
  8. 8. Microbiology Research Group, College of Pharmacy, Al-Ayen University, Thi-Qar, Iraq
  9. 9. Medical Laboratory Technology Department, College of Medical Technology, The Islamic University, Najaf, Iraq
  10. 10. Institute of Pharmaceutical Research, GLA University, UP, Mathura, 281406, India
  11. 11. Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
  12. 12. Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Pathology Research and Practice Published:2023


Abstract

NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome pathway has a critical role in the pathogenesis of atherosclerosis. Activation of this pathway is implicated in the subendothelial inflammation and atherosclerosis progression. The NLRP3 inflammasome are cytoplasmic sensors with the distinct capacity to identify a wide range of inflammation-related signals, which enhance NLRP3 inflammasome assembly and allow it to trigger inflammation. This pathway is triggered by a variety of intrinsic signals which exist in atherosclerotic plaques, like cholesterol crystals and oxidized LDL. Further pharmacological findings indicated that NLRP3 inflammasome enhanced caspase-1-mediated secretion of pro-inflammatory mediators like interleukin (IL)− 1β/18. Newly published cutting-edge studies suggested that non-coding RNAs (ncRNAs) including microRNAs (miRNAs, miRs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs) are major modulators of NLRP3 inflammasome in atherosclerosis. Therefore, in this review, we aimed to discuss the NLRP3 inflammasome pathway, biogenesis of ncRNAs as well as the modulatory role of ncRNAs in regulating the various mediators of NLRP3 inflammasome pathway including TLR4, NF-kB, NLRP3, and caspase 1. We also discussed the importance of NLRP3 inflammasome pathway-related ncRNAs as a diagnostic biomarker in atherosclerosis and current therapeutics in the modulation of NLRP3 inflammasome in atherosclerosis. Finally, we speak about the limitations and future prospects of ncRNAs in regulating inflammatory atherosclerosis via the NLRP3 inflammasome pathway. © 2023 Elsevier GmbH
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