ReviewAmerican journal of hypertension2017
Inflammation, Autoimmunity, and Hypertension: The Essential Role of Tissue Transglutaminase.
Review in American journal of hypertension, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Beyond neurotransmission: the roles of serotonylation in physiological and pathological processes.Cellular & molecular biology letters · 2026Review
- Detailed investigation of B cell populations following vaccination and infection with severe acute respiratory syndrome coronavirus-2 during pregnancy.Frontiers in immunology · 2026Article
- Renin-Angiotensin System Autoantibody Network in Parkinson's Disease Patients.Antioxidants (Basel, Switzerland) · 2025Article
- Serum angiotensin type-1 receptor autoantibodies and neurofilament light chain as markers of neuroaxonal damage in post-COVID patients.Frontiers in immunology · 2025Article
- Non-HLA angiotensin-type-1 receptor autoantibodies mediate the long-term loss of grafted neurons in Parkinson's disease models.Stem cell research & therapy · 2024Article
- Proteomic studies of VEGFR2 in human placentas reveal protein associations with preeclampsia, diabetes, gravidity, and labor.Cell communication and signaling : CCS · 2024Article
- Role of Serotonylation and SERT Posttranslational Modifications in Alzheimer's Disease Pathogenesis.Aging and disease · 2024Review
- Angiotensin type-1 receptor autoantibodies promote alpha-synuclein aggregation in dopaminergic neurons.Frontiers in immunology · 2024Article
- Cross-reactivity and sequence similarity between microbial transglutaminase and human tissue antigens.Scientific reports · 2023Article
- Inhibition of the ATAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Angiotensin type-1 receptor and ACE2 autoantibodies in Parkinson´s disease.NPJ Parkinson's disease · 2022Article
- Drugs Modulating Renin-Angiotensin System in COVID-19 Treatment.Biomedicines · 2022Review
- Evaluation of a Bi-Analyte Immunoblot as a Useful Tool for Diagnosing Dermatitis Herpetiformis.Diagnostics (Basel, Switzerland) · 2021Article
- Autoantibodies against ACE2 and angiotensin type-1 receptors increase severity of COVID-19.Journal of autoimmunity · 2021Article
- Association of non-HLA antibodies against endothelial targets and donor-specific HLA antibodies with antibody-mediated rejection and graft function in pediatric kidney transplant recipients.Pediatric nephrology (Berlin, Germany) · 2021Article
- Review
- Idiopathic pulmonary fibrosis and pulmonary hypertension: Heracles meets the Hydra.British journal of pharmacology · 2021Review
- Chemical Characterisation and Antihypertensive Effects of Locular Gel and Serum ofMolecules (Basel, Switzerland) · 2020Article
- Infection-driven activation of transglutaminase 2 boosts glucose uptake and hexosamine biosynthesis in epithelial cells.The EMBO journal · 2020Article
- Tissue Transglutaminase-Mediated AT1 Receptor Sensitization Underlies Pro-inflammatory Cytokine LIGHT-Induced Hypertension.American journal of hypertension · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory cytokines cause hypertension when introduced into animals. Additional evidence indicates that cytokines induce the production of autoantibodies that activate the AT1 angiotensin receptor (AT1R). Extensive evidence shows that these autoantibodies, termed AT1-AA, contribute to hypertension. We review here recent studies showing that cytokine-induced hypertension and AT1-AA production require the ubiquitous enzyme, tissue transglutaminase (TG2). We consider 3 mechanisms by which TG2 may contribute to hypertension. (i) One involves the posttranslational modification (PTM) of AT1Rs at a glutamine residue that is present in the epitope sequence (AFHYESQ) recognized by AT1-AA. (ii) Another mechanism by which TG2 may contribute to hypertension is by PTM of AT1Rs at glutamine 315. Modification at this glutamine prevents ubiquitination-dependent proteasome degradation and allows AT1Rs to accumulate. Increased AT1R abundance is likely to account for increased sensitivity to Ang II activation and in this way contribute to hypertension. (iii) The increased TG2 produced as a result of elevated inflammatory cytokines is likely to contribute to vascular stiffness by modification of intracellular contractile proteins or by crosslinking vascular proteins in the extracellular matrix. This process, termed inward remodeling, results in reduced vascular lumen, vascular stiffness, and increased blood pressure. Based on the literature reviewed here, we hypothesize that TG2 is an essential participant in cytokine-induced hypertension. From this perspective, selective TG2 inhibitors have the potential to be pharmacologic weapons in the fight against hypertension.
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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.