ArticleOncotarget2016
Instigation of NLRP3 inflammasome activation and glomerular injury in mice on the high fat diet: role of acid sphingomyelinase gene.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Podocyte-specific acid sphingomyelinase overexpression promotes gasdermin D dependent pyroptosis by impairing autophagic flux during obesity.Frontiers in physiology · 2026Article
- Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025Review
- Acid Sphingomyelinase and Ceramide Signaling Pathway Mediates Nicotine-Induced NLRP3 Inflammasome Activation and Podocyte Injury.Biomedicines · 2025Article
- Podocyte-specific silencing of acid sphingomyelinase gene to abrogate hyperhomocysteinemia-induced NLRP3 inflammasome activation and glomerular inflammation.American journal of physiology. Renal physiology · 2024Article
- Immunolocalization of Sphingolipid Catabolism Enzymes along the Nephron: Novel Early Urinary Biomarkers of Renal Damage.International journal of molecular sciences · 2023Article
- Regulation of NLRP3 Inflammasome Activation and Inflammatory Exosome Release in Podocytes by Acid Sphingomyelinase During Obesity.Inflammation · 2023Article
- Article
- Bisdemethoxycurcumin Attenuated Renal Injury via Activation of Keap1/Nrf2 Pathway in High-Fat Diet-Fed Mice.International journal of molecular sciences · 2022Article
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Effect of Empagliflozin on Sphingolipid Catabolism in Diabetic and Hypertensive Rats.International journal of molecular sciences · 2022Article
- Article
- Lipid regulation of NLRP3 inflammasome activity through organelle stress.Trends in immunology · 2021Review
- Podocyte Sphingolipid Signaling in Nephrotic Syndrome.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Review
- Abnormal podocyte TRPML1 channel activity and exosome release in mice with podocyte-specific Asah1 gene deletion.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021Article
- Release and Actions of Inflammatory Exosomes in Pulmonary Emphysema: Potential Therapeutic Target of Acupuncture.Journal of inflammation research · 2021Article
- Inflammasome activation in podocytes: a new mechanism of glomerular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Podocytopathy and Nephrotic Syndrome in Mice with Podocyte-Specific Deletion of the Asah1 Gene: Role of Ceramide Accumulation in Glomeruli.The American journal of pathology · 2020Article
- Acid sphingomyelinase deficiency exacerbates LPS-induced experimental periodontitis.Oral diseases · 2020Article
- Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ceramide has been reported to initiate inflammasome formation and activation in obesity and different pathological conditions. The present study was performed to explore the role of acid sphingomyelinase (Asm) in the development of high fat diet (HFD)-induced inflammasome and activation and consequent glomerular injury. Asm knockout (Asm(-/-)) and wild type (Asm(+/+)) mice with or without Asm short hairpin RNA (shRNA) transfection were fed a HFD or normal chow for 12 weeks to produce obesity and associated glomerular injury. HFD significantly enhanced the Asm activity, ceramide production, colocalization of Nlrp3 (Nod-like receptor protein 3) with ASC (apoptosis-associated speck-like protein) or Caspase-1, NADPH-dependent superoxide (O2(•-)) production in glomeruli of Asm(+/+) mice than in control diet-fed mice. However, such HFD-induced increases in Asm activity, ceramide production, colocalization of Nlrp3 with ASC or Caspase-1, superoxide (O(2•-)) production was attenuated in Asm(-/-) or Asm shRNA-transfected wild-type mice. In consistency with decreased inflammasome formation, the caspase-1 activity and IL-1β production was significantly attenuated in Asm(-/-) or Asm shRNA-transfected wild-type mice fed a HFD. Morphological examinations showed that HFD-induced profound injury in glomeruli of Asm(+/+) mice which was markedly attenuated in Asm(-/-) mice. The decreased glomerular damage index in Asm(-/-) mice was accompanied by attenuated proteinuria. Fluorescent immunohistochemical examinations using podocin as a podocyte marker showed that inflammasome formation induced by the HFD were mostly located in podocytes as demonstrated by co-localization of podocin with Nlrp3. In conclusion, these observations disclose a pivotal role of Asm in the HFD-induced inflammasome formation and consequent glomerular inflammation and injury.
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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.