ArticleSignal transduction and targeted therapy2021
CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice.
Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 73 citations in OpenAlex.
- MTR4 deficiency attenuates abdominal aortic aneurysm progression through suppressing VSMC senescence via the MTR4-RAP1a axis.iScience · 2026Article
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis.Circulation research · 2026Article
- Circulating CD38 shows stronger association with incident heart failure in women despite lower levels: sex differences and kidney-function context.Biology of sex differences · 2026Article
- Tacrolimus Induced Hypertension and Vascular Remodeling Includes Mechanisms of Cellular Senescence-The Protective Effect of Valsartan.Acta physiologica (Oxford, England) · 2026Article
- Double-Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration.Aging cell · 2026 · on this mapArticle
- Ginsenoside Rb1 Targets the HRD1-STING Axis to Mitigate Cholesterol-Induced VSMC Senescence.Journal of clinical laboratory analysis · 2026Article
- Review
- Research progress on targeted regulatory proteins in the prevention and treatment of atherosclerosis.Frontiers in immunology · 2026Review
- Macrophage Trem2 deficiency aggravates aging-induced vascular remodeling by acting as a non-classical receptor of interleukin-13.Molecular biomedicine · 2025Article
- KDM4A-induced tumor senescence enhances the efficacy of immunotherapy by inhibiting AGT-PHB1 axis-mediated mitophagy in colorectal cancer.Autophagy · 2025Article
- Intermedin Inhibits DNA Damage-Promoted Senescent Phenotype Transition of Vascular Smooth Muscle Cells in Aorta by Activating NAMPT/PARP1 in Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- Decreased PECAM-1 May be a potential pathological factor for vascular injury in T2DM patients.Scientific reports · 2025Article
- The Role of NADAmerican journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- Nicotinamide Mononucleotide (NMN) Improves the Senescence of Mouse Vascular Smooth Muscle Cells Induced by Ang II Through Activating p-AMPK/KLF4 Pathway.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Endothelial FOSL1 drives angiotensin II-induced myocardial injury via AT1R-upregulated MYH9.Acta pharmacologica Sinica · 2025Article
- Multifunctional hydrogel targeting senescence to accelerate diabetic wound healing through promoting angiogenesis.Journal of nanobiotechnology · 2025Article
- Targeting NAMPT-OPA1 for treatment of senile osteoporosis.Aging cell · 2025Article
- USP25 ameliorates vascular remodeling by deubiquitinating FOXO3 and promoting autophagic degradation of FOXO3.Acta pharmaceutica Sinica. B · 2025Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells. Decreased NAD levels are closely related to metabolic syndromes and aging-related diseases. Our study showed that CD38 deficiency significantly alleviated angiotensin II (Ang II)-induced vascular remodeling in mice, as shown by decreased blood pressures; reduced vascular media thickness, media-to-lumen ratio, and collagen deposition; and restored elastin expression. However, our bone marrow transplantation assay showed that CD38 deficiency in lymphocytes led to lack of protection against Ang II-induced vascular remodeling, suggesting that the effects of CD38 on Ang II-induced vascular remodeling might rely primarily on vascular smooth muscle cells (VSMCs), not lymphocytes. In addition, we observed that CD38 deficiency or NAD supplementation remarkably mitigated Ang II-induced vascular senescence by suppressing the biogenesis, secretion, and internalization of senescence-associated small extracellular vesicles (SA-sEVs), which facilitated the senescence of neighboring non-damaged VSMCs. Furthermore, we found that the protective effects of CD38 deficiency on VSMC senescence were related to restoration of lysosome dysfunction, particularly with respect to the maintenance of sirtuin-mediated mitochondrial homeostasis and activation of the mitochondria-lysosomal axis in VSMCs. In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling.
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