ArticleThe Journal of biological chemistry2010
CD38-mediated Ca2+ signaling contributes to angiotensin II-induced activation of hepatic stellate cells: attenuation of hepatic fibrosis by CD38 ablation.
Article in The Journal of biological chemistry, 2010. 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, 65 citations in OpenAlex.
- Article
- Lactylation Genes LDHA and LDHC Alleviate Osteoarthritis by Reducing Specific B-Cell Expression: Mechanistic Exploration and Experimental Validation.Journal of cellular and molecular medicine · 2025Article
- Robinetin Alleviates Metabolic Failure in Liver through Suppression of p300-CD38 Axis.Biomolecules & therapeutics · 2024Article
- Enzymology of CaCells · 2023Review
- NAADP-Mediated CaHandbook of experimental pharmacology · 2023Article
- Role of Liver CD38 in the Regulation of Metabolic Pathways during Cold-Induced Thermogenesis in Mice.Cells · 2022Article
- Possible Role of Extracellular Vesicles in Hepatotoxicity of Acetaminophen.International journal of molecular sciences · 2022Article
- CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.EMBO molecular medicine · 2022Article
- Promising Antigens for the New Frontier of Targeted Immunotherapy in Multiple Myeloma.Cancers · 2021Review
- CD38 in the age of COVID-19: a medical perspective.Physiological reviews · 2021Review
- Intermittent Hypoxia Upregulates theInternational journal of molecular sciences · 2021Article
- Zinc Administration and Improved Serum Markers of Hepatic Fibrosis in Patients with Autoimmune Hepatitis.Journal of clinical medicine · 2021Article
- Targeting CD38 is lethal to Breg-like chronic lymphocytic leukemia cells and Tregs, but restores CD8+ T-cell responses.Blood advances · 2020Article
- CD38: An Immunomodulatory Molecule in Inflammation and Autoimmunity.Frontiers in immunology · 2020Review
- Nicotinamide riboside, an NAD+ precursor, attenuates the development of liver fibrosis in a diet-induced mouse model of liver fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- CD38 affects the biological behavior and energy metabolism of nasopharyngeal carcinoma cells.International journal of oncology · 2019Article
- New Concepts on Reversibility and Targeting of Liver Fibrosis; A Review Article.Middle East journal of digestive diseases · 2018Article
- Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span.The Journal of experimental medicine · 2017Article
- Ion channels in control of pancreatic stellate cell migration.Oncotarget · 2017Article
- A novel mechanism underlies atrazine toxicity in quails (Coturnix Coturnix coturnix): triggering ionic disorder via disruption of ATPases.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD38 is a type II glycoprotein that is responsible for the synthesis and hydrolysis of cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), Ca(2+)-mobilizing second messengers. The activation of hepatic stellate cells (HSCs) is a critical event in hepatic fibrosis because these cells are the main producers of extracellular matrix proteins in the liver. Recent evidence indicates that the renin-angiotensin system plays a major role in liver fibrosis. In this study, we showed that angiotensin II (Ang II) evoked long lasting Ca(2+) rises and induced NAADP or cADPR productions via CD38 in HSCs. Inositol 1,4,5-trisphosphate as well as NAADP-induced initial Ca(2+) transients were prerequisite for the production of cADPR, which was responsible for later sustained Ca(2+) rises in the Ang II-treated HSCs. Ang II-mediated inositol 1,4,5-trisphosphate- and NAADP-stimulated Ca(2+) signals cross-talked in a dependent manner with each other. We also demonstrated that CD38 plays an important role in Ang II-induced proliferation and overproduction of extracellular matrix proteins in HSCs, which were reduced by an antagonistic cADPR analog, 8-bromo-cADPR, or in CD38(-/-) HSCs. Moreover, we presented evidence to implicate CD38 in the bile duct ligation-induced liver fibrogenesis; infiltration of inflammatory cells and expressions of alpha-smooth muscle actin, transforming growth factor-beta1, collagen alphaI(1), and fibronectin were reduced in CD38(-/-) mice compared with those in CD38(+/+) mice. These results demonstrate that CD38-mediated Ca(2+) signals contribute to liver fibrosis via HSCs activation, suggesting that intervention of CD38 activation may help prevent hepatic fibrosis.
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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.