Sphingolipid Metabolism and Signaling in Health and Diseases: 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 738

Special Issue Editors


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Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Interests: sphingolipids; neurodegenerative disorders; GM1 ganglioside; lysosomes
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Interests: glycosphingolipids; gangliosides; GM1; GM1 oligosaccharide; plasma membrane signaling; neuronal disease; Parkinson’s disease
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Interests: gangliosides; GM1 ganglioside; neurodegenerative and neurodevelopmental disor-ders; mitochondria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Sphingolipids are a class of lipids highly expressed in eukaryotic cells, where they represent key components of membranes. In addition to their structural role, they act as bioactive molecules capable of modulating intracellular signaling and, accordingly, several cell functions, including cell proliferation, differentiation, migration and apoptosis. Consequently, alterations in sphingolipid metabolism and signaling have been associated with several pathological conditions, spanning from neurodegeneration to cancer and diabetes. However, a complete comprehension of the molecular mechanism by which sphingolipids regulate cell homeostasis is still lacking. Providing new information about sphingolipid signaling and metabolism is pivotal for addressing their role both in health and in diseases.

In this Special Issue “Sphingolipid Metabolism and Signaling in Health and Disease”, we aim to collect original research and review articles regarding the role of sphingolipids in modulating cellular functions in different physiopathological conditions.

Dr. Giulia Lunghi
Dr. Elena Chiricozzi
Dr. Maria Fazzari
Guest Editors

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Keywords

  • sphingolipids
  • glycosphingolipids
  • gangliosides
  • sphingosine-1-phosphate
  • cell homeostasis
  • neurodegeneration
  • neurodevelopment
  • inflammation
  • diabetes
  • cystic fibrosis
  • cancer

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Published Papers (1 paper)

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Research

19 pages, 3499 KiB  
Article
Acid Sphingomyelinase and Ceramide Signaling Pathway Mediates Nicotine-Induced NLRP3 Inflammasome Activation and Podocyte Injury
by Mohammad Atiqur Rahman, Sayantap Datta, Harini Lakkakula, Saisudha Koka and Krishna M. Boini
Biomedicines 2025, 13(2), 416; https://doi.org/10.3390/biomedicines13020416 - 9 Feb 2025
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Abstract
Background: Recent studies have shown that Nlrp3 inflammasome activation is importantly involved in podocyte dysfunction induced by nicotine. The present study was designed to test whether acid sphingomyelinase (Asm) and ceramide signaling play a role in mediating nicotine-induced Nlrp3 inflammasome activation and subsequent [...] Read more.
Background: Recent studies have shown that Nlrp3 inflammasome activation is importantly involved in podocyte dysfunction induced by nicotine. The present study was designed to test whether acid sphingomyelinase (Asm) and ceramide signaling play a role in mediating nicotine-induced Nlrp3 inflammasome activation and subsequent podocyte damage. Methods and Results: Nicotine treatment significantly increased the Asm expression and ceramide production compared to control cells. However, prior treatment with amitriptyline, an Asm inhibitor significantly attenuated the nicotine-induced Asm expression and ceramide production. Confocal microscopic and biochemical analyses showed that nicotine treatment increased the colocalization of NLRP3 with Asc, Nlrp3 vs. caspase-1, IL-1? production, caspase-1 activity, and desmin expression in podocytes compared to control cells. Pretreatment with amitriptyline abolished the nicotine-induced colocalization of NLRP3 with Asc, Nlrp3 with caspase-1, IL-1? production, caspase-1 activity and desmin expression. Immunofluorescence analyses showed that nicotine treatment significantly decreased the podocin expression compared to control cells. However, prior treatment with amitriptyline attenuated the nicotine-induced podocin reduction. In addition, nicotine treatment significantly increased the cell permeability, O2 production, and apoptosis compared to control cells. However, prior treatment with amitriptyline significantly attenuated the nicotine-induced cell permeability, O2 production and apoptosis in podocytes. Conclusions: Asm is one of the important mediators of nicotine-induced inflammasome activation and podocyte injury. Asm may be a therapeutic target for the treatment or prevention of glomerulosclerosis associated with smoking. Full article
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