ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Physiological cyclic strain promotes endothelial cell survival via the induction of heme oxygenase-1.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- Acute and chronic effects of resistance training on skeletal muscle markers of mitochondrial remodeling in older adults.Physiological reports · 2020Trial
- Hypertensive stretch regulates endothelial cell inflammation and apoptosis through ceramide metabolism.American journal of physiology. Cell physiology · 2026Article
- Selective Inhibition of Vascular Smooth Muscle Cell Function by COVID-19 Antiviral Drugs: Impact of Heme Oxygenase-1.Antioxidants (Basel, Switzerland) · 2025Article
- Tug of war: Understanding the dynamic interplay of tumor biomechanical environment on dendritic cell function.Mechanobiology in medicine · 2024Review
- Considering the Influence of Coronary Motion on Artery-Specific Biomechanics Using Fluid-Structure Interaction Simulation.Annals of biomedical engineering · 2023Article
- Receptor-Ligand Binding: Effect of Mechanical Factors.International journal of molecular sciences · 2023Review
- Glutamine Deficiency Promotes Immune and Endothelial Cell Dysfunction in COVID-19.International journal of molecular sciences · 2023Review
- Building Blood Vessel Chips with Enhanced Physiological Relevance.Advanced materials technologies · 2023Article
- Endothelial Dysfunction in Patients with Advanced Heart Failure Treated with Levosimendan Periodic Infusion Compared with Optimal Medical Therapy: A Pilot Study.Life (Basel, Switzerland) · 2022Article
- Canagliflozin Inhibits Human Endothelial Cell Inflammation through the Induction of Heme Oxygenase-1.International journal of molecular sciences · 2022Article
- 3D Tissue-Engineered Vascular Drug Screening Platforms: Promise and Considerations.Frontiers in cardiovascular medicine · 2022Review
- Continuous flow left ventricular assist devices do not worsen endothelial function in subjects with chronic heart failure: a pilot study.ESC heart failure · 2021Article
- From arteries to capillaries: approaches to engineering human vasculature.Advanced functional materials · 2020Article
- Canagliflozin inhibits vascular smooth muscle cell proliferation and migration: Role of heme oxygenase-1.Redox biology · 2020Article
- Biofabrication Strategies and Engineered In Vitro Systems for Vascular Mechanobiology.Advanced healthcare materials · 2020Review
- Article
- The Nrf2 activator RTA-408 attenuates osteoclastogenesis by inhibiting STING dependent NF-κb signaling.Redox biology · 2020Article
- Review
- Tanshinone IIA attenuates ovalbumin-induced airway inflammation and hyperresponsiveness in a murine model of asthma.Iranian journal of basic medical sciences · 2019Article
- Canagliflozin Inhibits Human Endothelial Cell Proliferation and Tube Formation.Frontiers in pharmacology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial cells (ECs) are constantly subjected to cyclic strain that arises from periodic change in vessel wall diameter as a result of pulsatile blood flow. Application of physiological levels of cyclic strain inhibits EC apoptosis; however, the underlying mechanism is not known. Since heme oxygenase-1 (HO-1) is a potent inhibitor of apoptosis, the present study investigated whether HO-1 contributes to the antiapoptotic action of cyclic strain. Administration of physiological cyclic strain (6% at 1 Hz) to human aortic ECs stimulated an increase in HO-1 activity, protein, and mRNA expression. The induction of HO-1 was preceded by a rise in reactive oxygen species (ROS) and Nrf2 protein expression. Cyclic strain also stimulated an increase in HO-1 promoter activity that was prevented by mutating the antioxidant responsive element in the promoter or by overexpressing dominant-negative Nrf2. In addition, the strain-mediated induction of HO-1 and activation of Nrf2 was abolished by the antioxidant N-acetyl-l-cysteine. Finally, application of cyclic strain blocked inflammatory cytokine-mediated EC death and apoptosis. However, the protective action of cyclic strain was reversed by the HO inhibitor tin protoporphyrin-IX and was absent in ECs isolated from HO-1-deficient mice. In conclusion, the present study demonstrates that a hemodynamically relevant level of cyclic strain stimulates HO-1 gene expression in ECs via the ROS-Nrf2 signaling pathway to inhibit EC death. The ability of cyclic strain to induce HO-1 expression may provide an important mechanism by which hemodynamic forces promote EC survival and vascular homeostasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.