ArticleCell death & disease2016
Neutral sphingomyelinase (SMPD3) deficiency disrupts the Golgi secretory pathway and causes growth inhibition.
Article in Cell death & disease, 2016. 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, 46 citations in OpenAlex.
- Dysregulation of Sphingolipid Metabolism in Non-Obstructive Azoospermia: Insights from Bioinformatics and a Busulfan-Induced Mouse Model.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Unraveling the pathogenic mechanisms of osteoarthritis and obesity: An integration of GWAS, cellular specificity, and spatial transcriptomics.Osteoarthritis and cartilage open · 2026Article
- ASAH2 deficiency affects sphingolipid homeostasis and neuromotor control, causing a progressive neurological disorder.HGG advances · 2026Article
- Sphingomyelin phosphodiesterase 3 as a novel host factor inhibiting hepatitis B virus transcription.Virologica Sinica · 2025Article
- SMPD3 as a Potential Biomarker and Therapeutic Target in Hepatocellular Carcinoma.International journal of genomics · 2025Article
- A blood glucose fluctuation-responsive delivery system promotes bone regeneration and the repair function of Smpd3-reprogrammed BMSC-derived exosomes.International journal of oral science · 2024Article
- SMPD4-mediated sphingolipid metabolism regulates brain and primary cilia development.Development (Cambridge, England) · 2024Article
- Genome-wide variation study and inter-tissue communication analysis unveil regulatory mechanisms of egg-laying performance in chickens.Nature communications · 2024Article
- The Role of Neutral Sphingomyelinase-2 (NSM2) in the Control of Neutral Lipid Storage in T Cells.International journal of molecular sciences · 2024Article
- Analysis of the Selection Signal of the Tibetan Black Chicken Genome Based on Whole-Genome Sequencing.Genes · 2023Article
- Discovery of Orally Bioavailable and Brain-Penetrable Prodrugs of the Potent nSMase2 Inhibitor DPTIP.Journal of medicinal chemistry · 2022Article
- Small extracellular vesicle non-coding RNAs in pancreatic cancer: molecular mechanisms and clinical implications.Journal of hematology & oncology · 2021Review
- Neonatal stroke enhances interaction of microglia-derived extracellular vesicles with microglial cells.Neurobiology of disease · 2021Article
- Downregulation of ROR2 promotes dental pulp stem cell senescence by inhibiting STK4-FOXO1/SMS1 axis in sphingomyelin biosynthesis.Aging cell · 2021Article
- Exosomes: Emerging Cell-Free Based Therapeutics in Dermatologic Diseases.Frontiers in cell and developmental biology · 2021Review
- Loss of SMPD4 Causes a Developmental Disorder Characterized by Microcephaly and Congenital Arthrogryposis.American journal of human genetics · 2019Article
- Elucidating the transcriptional program of feline injection-site sarcoma using a cross-species mRNA-sequencing approach.BMC cancer · 2019Article
- Role of Neutral Sphingomyelinase-2 (NSM 2) in the Control of T Cell Plasma Membrane Lipid Composition and Cholesterol Homeostasis.Frontiers in cell and developmental biology · 2019Article
- Translational Approaches Targeting Ceramide Generation From Sphingomyelin in T Cells to Modulate Immunity in Humans.Frontiers in immunology · 2019Review
- Sphingomyelin Breakdown in T Cells: Role of Membrane Compartmentalization in T Cell Signaling and Interference by a Pathogen.Frontiers in cell and developmental biology · 2019Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic loss of neutral sphingomyelinase (SMPD3) in mice leads to a novel form of systemic, juvenile hypoplasia (dwarfism). SMPD3 deficiency in mainly two growth regulating cell types contributes to the phenotype, in chondrocytes of skeletal growth zones to skeletal malformation and chondrodysplasia, and in hypothalamic neurosecretory neurons to systemic hypothalamus-pituitary-somatotropic hypoplasia. The unbiased smpd3-/- mouse mutant and derived smpd3-/- primary chondrocytes were instrumental in defining the enigmatic role underlying the systemic and cell autonomous role of SMPD3 in the Golgi compartment. Here we describe the unprecedented role of SMPD3. SMPD3 deficiency disrupts homeostasis of sphingomyelin (SM), ceramide (Cer) and diacylglycerol (DAG) in the Golgi SMPD3-SMS1 (SM-synthase1) cycle. Cer and DAG, two fusogenic intermediates, modify the membrane lipid bilayer for the initiation of vesicle formation and transport. Dysproteostasis, unfolded protein response, endoplasmic reticulum stress and apoptosis perturb the Golgi secretory pathway in the smpd3-/- mouse. Secretion of extracellular matrix proteins is arrested in chondrocytes and causes skeletal malformation and chondrodysplasia. Similarly, retarded secretion of proteo-hormones in hypothalamic neurosecretory neurons leads to hypothalamus induced combined pituitary hormone deficiency. SMPD3 in the regulation of the protein vesicular secretory pathway may become a diagnostic target in the etiology of unknown forms of juvenile growth and developmental inhibition.
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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.