ArticleHypertension (Dallas, Tex. : 1979)2014
Endoplasmic reticulum stress contributes to aortic stiffening via proapoptotic and fibrotic signaling mechanisms.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 62 citations in OpenAlex.
- Inositol Requiring Enzyme 1α Mediates Hypertension and Vascular Remodeling.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Effects of chronic social defeat stress on behavior and cognition by activating the ERS-NLRP3 signaling pathway in adult mice.Metabolic brain disease · 2025Article
- Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024Review
- Social defeat stress induces liver injury by modulating endoplasmic reticulum stress in C57BL/6J mice.Scientific reports · 2024Article
- Huaju Xiaoji Formula Regulates ERS-lncMGC/miRNA to Enhance the Renal Function of Hypertensive Diabetic Mice with Nephropathy.Journal of diabetes research · 2024Article
- Hypertension and cellular senescence.Biogerontology · 2023Review
- Soluble and insoluble protein aggregates, endoplasmic reticulum stress, and vascular dysfunction in Alzheimer's disease and cardiovascular diseases.GeroScience · 2023Review
- ER stress mediates Angiotensin II-augmented innate immunity memory and facilitates distinct susceptibilities of thoracic from abdominal aorta to aneurysm development.Frontiers in immunology · 2023Article
- Endoplasmic Reticulum Chemical Chaperone 3-Hydroxy-2-Naphthoic Acid Reduces Angiotensin II-Induced Vascular Remodeling and Hypertension In Vivo and Protein Synthesis In Vitro.Journal of the American Heart Association · 2022Article
- Inhibition of Endoplasmic Reticulum Stress Improves Acetylcholine-Mediated Relaxation in the Aorta of Type-2 Diabetic Rats.Molecules (Basel, Switzerland) · 2022Article
- An update on angiotensin-converting enzyme 2 structure/functions, polymorphism, and duplicitous nature in the pathophysiology of coronavirus disease 2019: Implications for vascular and coagulation disease associated with severe acute respiratory syndrome coronavirus infection.Frontiers in microbiology · 2022Review
- Molecular Interactions of Arterial Hypertension in Its Target Organs.International journal of molecular sciences · 2021Review
- Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- miR-1283 Contributes to Endoplasmic Reticulum Stress in the Development of Hypertension Through the Activating Transcription Factor-4 (ATF4)/C/EBP-Homologous Protein (CHOP) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Vascular Stress Signaling in Hypertension.Circulation research · 2021Review
- Mitofusin-2: A New Mediator of Pathological Cell Proliferation.Frontiers in cell and developmental biology · 2021Review
- Alterations in the phosphodiesterase type 5 pathway and oxidative stress correlate with erectile function in spontaneously hypertensive rats.Journal of cellular and molecular medicine · 2020Article
- Targeting Molecular Mechanism of Vascular Smooth Muscle Senescence Induced by Angiotensin II, A Potential Therapy via Senolytics and Senomorphics.International journal of molecular sciences · 2020Review
- 78 kDa Glucose-Regulated Protein Attenuates Protein Aggregation and Monocyte Adhesion Induced by Angiotensin II in Vascular Cells.International journal of molecular sciences · 2020Article
- Social defeat stress induces myocardial injury by modulating inflammatory factors.The Journal of international medical research · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Vascular smooth muscle cell apoptosis and collagen synthesis contribute to aortic stiffening. A cellular signaling mechanism contributing to apoptotic and fibrotic events is endoplasmic reticulum (ER) stress. In this study, we tested the hypothesis that induction of ER stress in a normotensive rat would cause profibrotic and apoptotic signaling, thereby contributing to aortic stiffening. Furthermore, we hypothesized that inhibition of ER stress in an angiotensin II (Ang II) model of hypertension would improve aortic stiffening. Induction of ER stress with tunicamycin in normotensive Sprague-Dawley rats (10 μg/kg per day, osmotic pump, 28 days) caused an increase in systolic blood pressure (mm Hg; 160±5) compared with vehicle-treated (127±3) or tunicamycin-treated rats that were cotreated with ER stress inhibitor 4-phenylbutyric acid (100 mg/kg per day, 28 days, [124±6]). There was an increase in aortic apoptosis (fold; 3.0±0.3), collagen content (1.4±0.1), and fibrosis (2.0±0.1) in the tunicamycin-treated rats compared with vehicle-treated rats. Inhibition of ER stress in male Sprague-Dawley rats given Ang II (60 ng/min, osmotic pump, 28 days) and treated with either tauroursodeoxycholic acid or phenylbutyric acid (100 mg/kg per day, i.p., 28 days) led to a 20 mm Hg decrease in blood pressure with either inhibitor compared with Ang II treatment alone. Aortic apoptosis, increased collagen content, and fibrosis in Ang II-treated rats were attenuated with ER stress inhibition. We conclude that ER stress is a new signaling mechanism that contributes to aortic stiffening via promoting apoptosis and fibrosis.
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Registered trials
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