ArticleJournal of molecular medicine (Berlin, Germany)2020
A cytosolic heat shock protein 90 and co-chaperone p23 complex activates RIPK3/MLKL during necroptosis of endothelial cells in acute respiratory distress syndrome.
Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Precision tumor targeting: gamma-irradiated ellagic acid therapy for ferroptosis and necroptosis modulation via GPX4/ALOX/RIPK/MLKL pathway inhibition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Melatonin alleviates sepsis-induced acute lung injury by inhibiting necroptosis via reducing circulating mtDNA release.Molecular medicine (Cambridge, Mass.) · 2025Article
- Integrating bulk, single-cell, and spatial transcriptomics to identify and functionally validate novel targets to enhance immunotherapy in NSCLC.NPJ precision oncology · 2025Article
- Emerging role of PANoptosis in kidney diseases: molecular mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2025Review
- Acute lung injury: a view from the perspective of necroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Bisphenol A Regulates the TNFR1 Pathway and Excessive ROS Mediated by miR-26a-5p/ADAM17 Axis to Aggravate Selenium Deficiency-Induced Necroptosis in Broiler Veins.Biological trace element research · 2024Article
- A Razor's Edge: Vascular Responses to Acute Inflammatory Lung Injury/Acute Respiratory Distress Syndrome.Annual review of physiology · 2024Review
- Prognostic Impact of Heat Shock Protein 90 Expression in Women Diagnosed with Cervical Cancer.International journal of molecular sciences · 2024Article
- Targeting ferroptosis opens new avenues in gliomas.International journal of biological sciences · 2024Review
- LncRNA MALAT1 Promoted Neuronal Necroptosis in Cerebral Ischemia-reperfusion Mice by Stabilizing HSP90.Neurochemical research · 2023Article
- RIPK1 inhibition contributes to lysosomal membrane stabilization in ischemic astrocytes via a lysosomal Hsp70.1B-dependent mechanism.Acta pharmacologica Sinica · 2023Article
- Role of necroptosis in kidney health and disease.Nature reviews. Nephrology · 2023Review
- RIPK1 in the inflammatory response and sepsis: Recent advances, drug discovery and beyond.Frontiers in immunology · 2023Review
- Breaking bad: necroptosis in the pathogenesis of gastrointestinal diseases.Frontiers in immunology · 2023Review
- HSP90 mediates the connection of multiple programmed cell death in diseases.Cell death & disease · 2022Review
- The role of necroptosis in common respiratory diseases in children.Frontiers in pediatrics · 2022Review
- Necroptosis Plays a Crucial Role in Vascular Injury during DVT and Is Enhanced by IL-17B.Journal of immunology research · 2022Article
- L-Carnitine ameliorates the liver by regulating alpha-SMA, iNOS, HSP90, HIF-1alpha, and RIP1 expressions of CCL4-toxic rats.Iranian journal of basic medical sciences · 2021Article
- Necroptosis in Pulmonary Diseases: A New Therapeutic Target.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necrosis with inflammation plays a crucial role in acute respiratory distress syndrome (ARDS). Receptor-interacting protein 3 (RIPK3) regulates a newly discovered programmed form of necrosis called necroptosis. However, the underlying mechanism of necroptosis in ARDS remains unknown. Thus, the purpose of this study was to examine the possible involvement of RIPK3 in ARDS-associated necroptosis. RIPK3 protein levels were found to be significantly elevated in the plasma and bronchoalveolar lavage fluid of ARDS patients. Next, we utilised a mouse model of severe ARDS induced with high-dose lipopolysaccharide and found that lung injury was mainly due to RIPK3-mixed lineage kinase domain-like pseudokinase (MLKL)-mediated necroptosis and endothelial dysfunction. The activation of RIPK3-MLKL by tumour necrosis factor receptor 1 (TNFR1) and TNFR1-associated death domain protein (TRADD) required catalytically active RIPK1 and the inhibition of Fas-associated protein with death domain (FADD)/caspase-8 catalytic activity. We further showed that the molecular chaperone heat shock protein 90 (Hsp90)/p23, as a novel RIPK3- and MLKL-interacting complex, played an important role in RIP-MLKL-mediated necroptosis, inflammation and endothelial dysfunction in the pulmonary vasculature, which resulted in ARDS. Collectively, the results of our study indicate that necroptosis is an important mechanism of cell death in ARDS and the inhibition of necroptosis may be a therapeutic intervention for ARDS. KEY MESSAGES: Lung injury in high-dose LPS-induced severe ARDS is mainly due to RIP3-MLKL-mediated necroptosis and endothelial dysfunction. Chaperone HSP90/p23 is a novel RIP3- and MLKL-interacting complex in HPAECs. HSP90/p23 is a novel RIP3- and MLKL-interacting complex in RIP-MLKL-mediated necroptosis, inflammation and endothelial dysfunction.
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