ArticleCardiovascular research2014
LOX-1, mtDNA damage, and NLRP3 inflammasome activation in macrophages: implications in atherogenesis.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
64 citing papers in PubMed, 137 citations in OpenAlex.
- Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Inhibition in Type 2 Diabetes: Phase 1 Results.Journal of the American Heart Association · 2023Trial
- Oxidized mitochondrial DNA as a potential biomarker and mechanistic driver of autophagy-mitophagy dysregulation in pulmonary arterial hypertension: a narrative review.Molecular biology reports · 2026Review
- A human single-cell atlas identifies OLR1Nature genetics · 2026Article
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Mitochondrial DNA-Mediated Immune Activation After Resuscitation From Cardiac Arrest.Journal of the American Heart Association · 2026Article
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- EngineeringExtracellular vesicles and circulating nucleic acids · 2026Article
- Fat-targeted small molecule alleviates abnormal adipose tissue remodeling in obesity via SIRT3-driven mitophagy and inflammasome inhibition.Chinese medicine · 2025Article
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Mitochondrial destabilization in tendinopathy and potential therapeutic strategies.Journal of orthopaedic translation · 2024Review
- Is the endotoxin-complement cascade the major driver in lipedema?Trends in endocrinology and metabolism: TEM · 2024Review
- Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis.Cardiovascular drugs and therapy · 2024Review
- NLRP3 inflammasome: a key player in the pathogenesis of life-style disorders.Experimental & molecular medicine · 2024Review
- LOX-1 in Cardiovascular Disease: A Comprehensive Molecular and Clinical Review.International journal of molecular sciences · 2024Review
- Radical Oxygen Species, Oxidized Low-Density Lipoproteins, and Lectin-like Oxidized Low-Density Lipoprotein Receptor 1: A Vicious Circle in Atherosclerotic Process.Antioxidants (Basel, Switzerland) · 2024Review
- Comprehensive view of macrophage autophagy and its application in cardiovascular diseases.Cell proliferation · 2024Review
- NLRP3 and autophagy in retinal ganglion cell inflammation in age-related macular degeneration: potential therapeutic implications.International journal of ophthalmology · 2024Review
- Unraveling the role of NLRP3 inflammasome in allergic inflammation: implications for novel therapies.Frontiers in immunology · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsLectin-like ox-LDL scavenger receptor-1 (LOX-1) and mitochondrial DNA (mtDNA) damage play a key role in a variety of cardiovascular diseases, including atherosclerosis, hypertension, and inflammation. We posited that damaged mtDNA could trigger autophagy and NLRP3 inflammasome activation, and LOX-1 may play a critical role in this process. METHODS AND
resultsIn order to examine this hypothesis, cultured human THP-1 macrophages exposed to lipopolysaccharide (LPS) were applied to study the link between LOX-1, mtDNA damage, autophagy, and NLRP3 inflammasome expression. Our data showed that LPS markedly induced LOX-1 expression, reactive oxygen species (ROS) generation, autophagy, mtDNA damage, and NLRP3 inflammasome. LOX-1 inhibition with a binding antibody or siRNA inhibited ROS generation, autophagy and mtDNA damage, and a decreased expression of NLRP3 inflammasome. To study the LOX-1-NLRP3 inflammasome signalling, we performed studies using ROS inhibitors and an autophagy inducer, and found that both decreased the expression of NLRP3. On the other hand, autophagy inhibitor enhanced the expression of NLRP3 inflammasome. Knockdown of DNase II inhibited autophagy and NLRP3 inflammasome, providing further support for our hypothesis. Finally, we confirmed the relationship between LOX-1, ROS, mtDNA damage, autophagy, and NLRP3 inflammasome activation in primary macrophages.
conclusionsThis study based on THP-1 macrophages and primary macrophages indicates that LOX-1-mediated autophagy and mtDNA damage play an essential role in NLRP3 inflammasome activation in inflammatory disease states.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.