ArticleThe Journal of clinical investigation2014
DC isoketal-modified proteins activate T cells and promote hypertension.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 364 papers.
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Who cites it
364 citing papers in PubMed, 525 citations in OpenAlex.
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- Beyond the guidelines: Vascular function as the central determinant and therapeutic target in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- High-Salt Diet Exacerbates Murine Imiquimod-Induced Psoriasis-like Dermatitis via Activation of Serum- and Glucocorticoid-Inducible Kinase 1.International journal of molecular sciences · 2026Article
- Myeloid Activator Protein-1 Complex Contributes to Salt-Sensitive Hypertension.Circulation research · 2026Article
- Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.Journal of the American Heart Association · 2026Article
- Metabolic-inflammatory memory: the common pathological basis and therapeutic targets of metabolic syndrome.Reviews in endocrine & metabolic disorders · 2026Review
- High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications.Chinese medical journal · 2026Review
- Conditional ablation of RGS2 in myeloid cells does not influence blood pressure and organ damage in angiotensin II-induced hypertension in mice.Physiological reports · 2026Article
- Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.Clinical science (London, England : 1979) · 2026Review
- Myeloid transglutaminase 2 regulates Treg-Th17 balance in a female model of angiotensin II-induced hypertension and vascular stiffening.American journal of physiology. Heart and circulatory physiology · 2026Article
- Inflammatory factors and hypertensive nephropathy: A bidirectional 2-sample Mendelian randomization study.Medicine · 2026Article
- Gut Microbiota as a Mediator of Dietary Salt Effects on Blood Pressure.International journal of molecular sciences · 2026Review
- Associations of urinary isoprostanes with structural and load-dependent arterial stiffness: the Multi-Ethnic Study of Atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Development of immune-derived molecular markers for coronary heart disease via multimachine learning.iScience · 2026Article
- Antigen-Presenting Cell Isolevuglandins Link Salt Sensitivity of Blood Pressure to Insulin Resistance.The Journal of clinical endocrinology and metabolism · 2026Article
- Scavenging of Isolevuglandins Attenuates Neutrophil Migration and Neutrophil Extracellular Trap Formation in Systemic Lupus Erythematosus.ACR open rheumatology · 2026Article
- MyD88 in myeloid cells drives angiotensin II-induced vascular inflammation, is associated with prevalent heart failure, and predicts all-cause mortality in arterial hypertension.European heart journal open · 2026Article
- The role of vascular aging, bone marrow and immune system in hypertension.Cell death discovery · 2026Review
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Hypertension in idiopathic pulmonary fibrosis: evidence of immune and genetic links from clinical and genomic analyses.Respiratory research · 2025Article
304 more citing papers are in PubMed but not listed here.
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Authors and funding
29 authors at 5 institutions in 4 countries.
Funding
Abstract
Oxidative damage and inflammation are both implicated in the genesis of hypertension; however, the mechanisms by which these stimuli promote hypertension are not fully understood. Here, we have described a pathway in which hypertensive stimuli promote dendritic cell (DC) activation of T cells, ultimately leading to hypertension. Using multiple murine models of hypertension, we determined that proteins oxidatively modified by highly reactive γ-ketoaldehydes (isoketals) are formed in hypertension and accumulate in DCs. Isoketal accumulation was associated with DC production of IL-6, IL-1β, and IL-23 and an increase in costimulatory proteins CD80 and CD86. These activated DCs promoted T cell, particularly CD8+ T cell, proliferation; production of IFN-γ and IL-17A; and hypertension. Moreover, isoketal scavengers prevented these hypertension-associated events. Plasma F2-isoprostanes, which are formed in concert with isoketals, were found to be elevated in humans with treated hypertension and were markedly elevated in patients with resistant hypertension. Isoketal-modified proteins were also markedly elevated in circulating monocytes and DCs from humans with hypertension. Our data reveal that hypertension activates DCs, in large part by promoting the formation of isoketals, and suggest that reducing isoketals has potential as a treatment strategy for this disease.
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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.