ReviewInternational journal of molecular sciences2021
Acid Sphingomyelinase, a Lysosomal and Secretory Phospholipase C, Is Key for Cellular Phospholipid Catabolism.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Sphingolipids associate with the chlamydial nucleoid and mark developmental transitions in Chlamydia trachomatis.Nature communications · 2026Article
- Article
- Risperidone induces osteoporosis and neuropsychiatric treatment resistance via SMPD1-lysosome-mediated ferroptosis: dual rescue by active vitamin D analog ED-71.Journal of advanced research · 2026Article
- Contradictory Effects on Hepatocytes in ASMD.International journal of molecular sciences · 2026Review
- Endolysosomal Impact of Elevated Ceramide Levels Revealed by Optical and Ultrastructural Nanoprobing.ACS nano · 2026Article
- An mTORC2-Lipid Signaling Axis Controls Stress-Induced Organismal Death.Research square · 2026Article
- Macrophage-mediated nutrient recycling: evolutionary insights into the metabolic role of professional phagocytes.Frontiers in immunology · 2026Review
- Acid sphingomyelinase is a gatekeeper of placental labyrinthine architecture and function.Development (Cambridge, England) · 2025Article
- Reduction of sphingomyelinase activity associated with progranulin deficiency and frontotemporal dementia.Neurobiology of disease · 2025Article
- Ceramides in cardiovascular disease: emerging role as independent risk predictors and novel therapeutic targets.Cardiovascular research · 2025Review
- High-Resolution Mass Spectrometry Method for Targeted Screening and Monitoring of Fabry, Gaucher and ASMD Using Dried Blood Spots and Capitainers: Impact of Sample Matrix on Measurement Results.International journal of molecular sciences · 2025Article
- Using ultrasound and microbubble to enhance the effects of conventional cancer therapies in clinical settings.Cancer metastasis reviews · 2025Review
- Lysosome-associated CASM: from upstream triggers to downstream effector mechanisms.Frontiers in cell and developmental biology · 2025Review
- Neutral sphingomyelinase 2: A promising drug target for CNS disease.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Key Mechanisms in Lysosome Stability, Degradation and Repair.Molecular and cellular biology · 2025Review
- Sphingolipid metabolism and regulated cell death in malignant melanoma.Apoptosis : an international journal on programmed cell death · 2024Review
- Acidic sphingomyelinase interactions with lysosomal membranes and cation amphiphilic drugs: A molecular dynamics investigation.Computational and structural biotechnology journal · 2024Article
- Global and Targeted Metabolomics for Revealing Metabolomic Alteration in Niemann-Pick Disease Type C Model Cells.Metabolites · 2024Article
- Lithium carbonate revitalizes tumor-reactive CD8Nature immunology · 2024Article
- Acid sphingomyelinase as a pathological and therapeutic target in neurological disorders: focus on Alzheimer's disease.Experimental & molecular medicine · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Here, we present the main features of human acid sphingomyelinase (ASM), its biosynthesis, processing and intracellular trafficking, its structure, its broad substrate specificity, and the proposed mode of action at the surface of the phospholipid substrate carrying intraendolysosomal luminal vesicles. In addition, we discuss the complex regulation of its phospholipid cleaving activity by membrane lipids and lipid-binding proteins. The majority of the literature implies that ASM hydrolyses solely sphingomyelin to generate ceramide and ignores its ability to degrade further substrates. Indeed, more than twenty different phospholipids are cleaved by ASM in vitro, including some minor but functionally important phospholipids such as the growth factor ceramide-1-phosphate and the unique lysosomal lysolipid bis(monoacylglycero)phosphate. The inherited ASM deficiency, Niemann-Pick disease type A and B, impairs mainly, but not only, cellular sphingomyelin catabolism, causing a progressive sphingomyelin accumulation, which furthermore triggers a secondary accumulation of lipids (cholesterol, glucosylceramide, GM2) by inhibiting their turnover in late endosomes and lysosomes. However, ASM appears to be involved in a variety of major cellular functions with a regulatory significance for an increasing number of metabolic disorders. The biochemical characteristics of ASM, their potential effect on cellular lipid turnover, as well as a potential impact on physiological processes will be discussed.
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Registered trials
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