ArticleBioengineering & translational medicine2023
Activation of NR1H3 attenuates the severity of septic myocardial injury by inhibiting NLRP3 inflammasome.
Article in Bioengineering & translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Role of oxidative stress in sepsis: Mechanisms, pathways, and therapeutic strategies.Journal of pharmaceutical analysis · 2026Review
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Autophagy activation by the Becn1Brain, behavior, and immunity · 2026Article
- Protective functions of liver X receptor α on calcified aortic valve: involvement of regulating endoplasmic reticulum-mediated osteogenic differentiation.Cardiovascular research · 2025Article
- The causal relationship between emotions and osteoarthritis: A bidirectional Mendelian randomization study.Medicine · 2025Article
- PANAXADIOL SAPONIN ALLEVIATES LPS-INDUCED CARDIOMYOPATHY SIMILAR TO DEXAMETHASONE VIA IMPROVING MITOCHONDRIAL QUALITY CONTROL.Shock (Augusta, Ga.) · 2025Article
- Mechanisms and Targeted Therapeutic Strategies in Sepsis-Induced Myocardial Dysfunction: The Role of NLRP3 Inflammasome-Mediated Inflammation.Journal of inflammation research · 2025Review
- NLRP3 Inflammasome Targeting Offers a Novel Therapeutic Paradigm for Sepsis-Induced Myocardial Injury.Drug design, development and therapy · 2025Review
- Correction to "Activation of NR1H3 attenuates the severity of septic myocardial injury by inhibiting NLRP3 inflammasome".Bioengineering & translational medicine · 2024Article
- Putative Pharmacological Depression and Anxiety-Related Targets of Calcitriol Explored by Network Pharmacology and Molecular Docking.Pharmaceuticals (Basel, Switzerland) · 2024Article
- LncRNA DLEU1 contributes to the progression of septic myocardial dysfunction by targeting miR-381-3p.Central-European journal of immunology · 2024Article
- Activation of NR1H3 attenuates the severity of septic myocardial injury by inhibiting NLRP3 inflammasome.Bioengineering & translational medicine · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most sepsis deaths are due to the development of multiple organ failure, in which heart failure is a recognized manifestation of sepsis. To date, the role of liver X receptors α (NR1H3) in sepsis is still uncertain. Here, we hypothesized that NR1H3 mediates multiple essential sepsis-related signalings to attenuate septic heart failure. Adult male C57BL/6 or Balbc mice and HL-1 myocardial cell line were performed for in vivo and in vitro experiments, respectively. NR1H3 knockout mice or NR1H3 agonist T0901317 was applied to evaluate the impact of NR1H3 on septic heart failure. We found decreased myocardial expression levels of NR1H3-related molecules while increased NLRP3 level in septic mice. NR1H3 knockout worsensed cardiac dysfunction and injury in mice subjected to cecal ligation and puncture (CLP), in association with exacerbated NLRP3-mediated inflammation, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis-related markers. The administration of T0901317 reduced systemic infection and improve cardiac dysfunction in septic mice. Moreover, Co-IP assays, luciferase reporter assays, and chromatin immunoprecipitation analysis, confirmed that NR1H3 directly repressed NLRP3 activity. Finally, RNA-seq detection further clarified an overview of the roles of NR1H3 in sepsis. In general, our findings indicate that NR1H3 had a significant protective effect against sepsis and sepsis-induced heart failure.
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Registered trials
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.