ArticleClinical science (London, England : 1979)2015
Phosphodiesterase 1 regulation is a key mechanism in vascular aging.
Article in Clinical science (London, England : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Targeting the NO-cGMP axis in age-related vascular dysfunction: a systematic review and meta-analysis of preclinical animal studies.GeroScience · 2026Review
- Trigeminovascular calcitonin gene-related peptide release and peripheral vascular responses in a mouse model of accelerated aging: Implications for migraine.The journal of headache and pain · 2026Article
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Cyclic nucleotide phosphodiesterases as drug targets.Pharmacological reviews · 2025Review
- Phosphodiesterase in heart and vessels: from physiology to diseases.Physiological reviews · 2024Review
- The perspective of cAMP/cGMP signaling and cyclic nucleotide phosphodiesterases in aortic aneurysm and dissection.Vascular pharmacology · 2024Review
- Cardiac System during the Aging Process.Aging and disease · 2023Review
- Article
- The landscape of aging.Science China. Life sciences · 2022Review
- Soluble guanylate cyclase activator BAY 54-6544 improves vasomotor function and survival in an accelerated ageing mouse model.Aging cell · 2022Article
- Age Impairs Soluble Guanylyl Cyclase Function in Mouse Mesenteric Arteries.International journal of molecular sciences · 2021Article
- Role of phosphodiesterase 1 in the pathophysiology of diseases and potential therapeutic opportunities.Pharmacology & therapeutics · 2021Review
- Cyclic nucleotide phosphodiesterase 1C contributes to abdominal aortic aneurysm.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Effects of Acute and Chronic Selective Phosphodiesterase 1 Inhibition on Smooth Muscle Cell-Associated Aging Features.Frontiers in pharmacology · 2021Article
- Vascular Ageing Features Caused by Selective DNA Damage in Smooth Muscle Cell.Oxidative medicine and cellular longevity · 2021Article
- Type 5 phosphodiesterase (PDE5) and the vascular tree: From embryogenesis to aging and disease.Mechanisms of ageing and development · 2020Review
- Chronic Sildenafil Treatment Improves Vasomotor Function in a Mouse Model of Accelerated Aging.International journal of molecular sciences · 2020Article
- Selective Phosphodiesterase 1 Inhibitor BTTQ Reduces Blood Pressure in Spontaneously Hypertensive and Dahl Salt Sensitive Rats: Role of Peripheral Vasodilation.Frontiers in physiology · 2020Article
- Placental effects and transfer of sildenafil in healthy and preeclamptic conditions.EBioMedicine · 2019Article
- Determinants of pulse wave velocity trajectories from youth to young adulthood: the Georgia Stress and Heart Study.Journal of hypertension · 2019Article
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18 authors at 5 institutions in 3 countries.
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Abstract
Reduced nitric oxide (NO)/cGMP signalling is observed in age-related vascular disease. We hypothesize that this disturbed signalling involves effects of genomic instability, a primary causal factor in aging, on vascular smooth muscle cells (VSMCs) and that the underlying mechanism plays a role in human age-related vascular disease. To test our hypothesis, we combined experiments in mice with genomic instability resulting from the defective nucleotide excision repair gene ERCC1 (Ercc1(d/-) mice), human VSMC cultures and population genome-wide association studies (GWAS). Aortic rings of Ercc1(d/-) mice showed 43% reduced responses to the soluble guanylate cyclase (sGC) stimulator sodium nitroprusside (SNP). Inhibition of phosphodiesterase (PDE) 1 and 5 normalized SNP-relaxing effects in Ercc1(d/-) to wild-type (WT) levels. PDE1C levels were increased in lung and aorta. cGMP hydrolysis by PDE in lungs was higher in Ercc1(d/-) mice. No differences in activity or levels of cGMP-dependent protein kinase 1 or sGC were observed in Ercc1(d/-) mice compared with WT. Senescent human VSMC showed elevated PDE1A and PDE1C and PDE5 mRNA levels (11.6-, 9- and 2.3-fold respectively), which associated with markers of cellular senescence. Conversely, PDE1 inhibition lowered expression of these markers. Human genetic studies revealed significant associations of PDE1A single nucleotide polymorphisms with diastolic blood pressure (DBP; β=0.28, P=2.47×10(-5)) and carotid intima-media thickness (cIMT; β=-0.0061, P=2.89×10(-5)). In summary, these results show that genomic instability and cellular senescence in VSMCs increase PDE1 expression. This might play a role in aging-related loss of vasodilator function, VSMC senescence, increased blood pressure and vascular hypertrophy.
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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.