ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Pivotal role of JNK-dependent FOXO1 activation in downregulation of kallistatin expression by oxidative stress.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Exploring the potential application of roxadustat in chronic kidney disease-related osteoporosis based on the regulatory role of HIF-1α in bone metabolism.Histology and histopathology · 2026Review
- FoxO1 Alleviates the Mitochondrial ROS Levels Induced by α-Synuclein Preformed Fibrils in BV-2 Microglial Cells.Inflammation · 2025Article
- Kallistatin deficiency exacerbates neuronal damage after cardiac arrest.Scientific reports · 2024Article
- Kallistatin prevents ovarian hyperstimulation syndrome by regulating vascular leakage.Journal of cellular and molecular medicine · 2022Article
- Article
- The FOXO signaling axis displays conjoined functions in redox homeostasis and stemness.Free radical biology & medicine · 2021Review
- Functional crosstalk between myeloid Foxo1-β-catenin axis and Hedgehog/Gli1 signaling in oxidative stress response.Cell death and differentiation · 2021Article
- A transition to degeneration triggered by oxidative stress in degenerative disorders.Molecular psychiatry · 2021Review
- Inhibition on JNK Mimics Silencing of Wnt-11 Mediated Cellular Response in Androgen-Independent Prostate Cancer Cells.Biology · 2020Article
- Prdx6 Plays a Main Role in the Crosstalk Between Aging and Metabolic Sarcopenia.Antioxidants (Basel, Switzerland) · 2020Article
- Review
- Aconitase 2 inhibits the proliferation of MCF-7 cells promoting mitochondrial oxidative metabolism and ROS/FoxO1-mediated autophagic response.British journal of cancer · 2020Article
- Protective effect of silencing Stat1 on high glucose-induced podocytes injury via Forkhead transcription factor O1-regulated the oxidative stress response.BMC molecular and cell biology · 2019Article
- Bidirectional regulation of osteogenic differentiation by the FOXO subfamily of Forkhead transcription factors in mammalian MSCs.Cell proliferation · 2019Review
- Reduced Plasma Kallistatin Is Associated With the Severity of Coronary Artery Disease, and Kallistatin Treatment Attenuates Atherosclerotic Plaque Formation in Mice.Journal of the American Heart Association · 2018Article
- Mulberry Anthocyanin Extract Ameliorates Oxidative Damage in HepG2 Cells and Prolongs the Lifespan ofOxidative medicine and cellular longevity · 2017Article
- Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway.Oxidative medicine and cellular longevity · 2017Review
- Protective Role of Kallistatin in Vascular and Organ Injury.Hypertension (Dallas, Tex. : 1979) · 2016Review
- The Potential Role of Kallistatin in the Development of Abdominal Aortic Aneurysm.International journal of molecular sciences · 2016Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress has been shown to suppress endothelial nitric oxide synthase expression through activation of the transcription factor forkhead box O 1 (FOXO1) in cultured endothelial cells. We previously reported that circulating kallistatin levels are markedly reduced in rats with chronic oxidative organ damage. In this study, we investigated the potential role of oxidative stress in suppression of kallistatin expression via FOXO1 activation. In Dahl salt-sensitive (DSS) rats, we found that high salt intake induced a time-dependent correlation of increased thiobarbituric acid reactive substances (TBARS, an indicator of lipid peroxidation) with reduced serum kallistatin levels. Moreover, salt loading provoked an elevation of in situ aortic superoxide formation in association with reduced kallistatin levels. Expression of kallistatin was identified in cultured endothelial cells by immunocytochemistry and flow cytometry; however, H(2)O(2) dose-dependently lowered kallistatin mRNA and protein levels as determined by real-time PCR and Western blot, respectively. Downregulation of kallistatin synthesis by oxidative stress was restored by knockdown of FOXO1 expression with small-interfering RNA. H(2)O(2) rapidly induced FOXO1 nuclear translocation, but the effect was blocked by c-Jun NH(2)-terminal kinase (JNK) inhibitor. Inhibition of JNK by pharmacological inhibitor or small-interfering RNA reversed H(2)O(2)'s effect on kallistatin expression in endothelial cells. This study demonstrates that an inverse relationship exists between oxidative stress and kallistatin levels in the circulation and blood vessels and that kallistatin expression is negatively regulated by oxidative stress via JNK-dependent FOXO1 activation in cultured endothelial cells.
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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.