ReviewComprehensive Physiology2021
Innate Immune Cells and Hypertension: Neutrophils and Neutrophil Extracellular Traps (NETs).
Review in Comprehensive Physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Correlation analysis of systemic immune inflammation index with the occurrence and clinical outcomes of hypertension: a systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2025Pooled it
- Association between neutrophil percentage-to-albumin ratio and vascular cognitive impairment in patients with cerebrovascular disease: a cross-sectional study.BMC neurology · 2026Trial
- Spatiotemporal heterogeneity of neutrophil extracellular traps in hepatocellular carcinoma microenvironment and targeted therapy progress.Journal of translational medicine · 2026Review
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- Development and validation of a nomogram prediction model for coronary heart disease in diabetic patients: a study based on the 2011-2020 NHANES database.BMC cardiovascular disorders · 2025Article
- Type 2 inflammation and cardiometabolic disease in middle-aged adults.ERJ open research · 2025Article
- Role of Neutrophil Extracellular Traps in Hypertension and Their Impact on Target Organs.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- IgG/IgM-coated gut microbiota in schizophrenia: associations with inflammation disease activity.Frontiers in psychiatry · 2025Article
- Improvement of the Immunity System Through Sports: Novel Regulatory Mechanisms for Hypertension.Reviews in cardiovascular medicine · 2024Review
- Glycosaminoglycans: Participants in Microvascular Coagulation of Sepsis.Thrombosis and haemostasis · 2024Review
- Immune cells and hypertension.Immunologic research · 2024Review
- Article
- Gender differences in the relationship between the systemic immune-inflammation index and all-cause and cardiovascular mortality among adults with hypertension: evidence from NHANES 1999-2018.Frontiers in endocrinology · 2024Article
- Neutrophil extracellular traps in intracerebral hemorrhage: implications for pathogenesis and therapeutic targets.Metabolic brain disease · 2023Review
- Effects of Long-Term Intervention with Losartan, Aspirin and Atorvastatin on Vascular Remodeling in Juvenile Spontaneously Hypertensive Rats.Molecules (Basel, Switzerland) · 2023Article
- The aggregate index of systemic inflammation (AISI): a novel predictor for hypertension.Frontiers in cardiovascular medicine · 2023Article
- Development and validation of a nomogram for predicting all-cause mortality in American adult hypertensive populations.Frontiers in pharmacology · 2023Article
- Six Decades of History of Hypertension Research at the University of Toledo: Highlighting Pioneering Contributions in Biochemistry, Genetics, and Host-Microbiota Interactions.Current hypertension reports · 2022Review
- Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Uncontrolled immune system activation amplifies end-organ injury in hypertension. Nonetheless, the exact mechanisms initiating this exacerbated inflammatory response, thereby contributing to further increases in blood pressure (BP), are still being revealed. While participation of lymphoid-derived immune cells has been well described in the hypertension literature, the mechanisms by which myeloid-derived innate immune cells contribute to T cell activation, and subsequent BP elevation, remains an active area of investigation. In this article, we critically analyze the literature to understand how monocytes, macrophages, dendritic cells, and polymorphonuclear leukocytes, including mast cells, eosinophils, basophils, and neutrophils, contribute to hypertension and hypertension-associated end-organ injury. The most abundant leukocytes, neutrophils, are indisputably increased in hypertension. However, it is unknown how (and why) they switch from critical first responders of the innate immune system, and homeostatic regulators of BP, to tissue-damaging, pro-hypertensive mediators. We propose that myeloperoxidase-derived pro-oxidants, neutrophil elastase, neutrophil extracellular traps (NETs), and interactions with other innate and adaptive immune cells are novel mechanisms that could contribute to the inflammatory cascade in hypertension. We further posit that the gut microbiota serves as a set point for neutropoiesis and their function. Finally, given that hypertension appears to be a key risk factor for morbidity and mortality in COVID-19 patients, we put forth evidence that neutrophils and NETs cause cardiovascular injury post-coronavirus infection, and thus may be proposed as an intriguing therapeutic target for high-risk individuals. © 2021 American Physiological Society. Compr Physiol 11:1575-1589, 2021.
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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.