Molecular and cellular mechanisms in vascular injury in hypertension: role of angiotensin II – editorial review
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Bibliographic record
Abstract
Purpose of review Emerging evidence indicates that hypertension is a vascular disease associated with inflammation, induced through redox-sensitive mechanisms that are regulated by angiotensin II. This review focuses on the role of inflammation, oxidative stress and angiotensin II in vascular injury and discusses implications of these processes in hypertension. Recent findings The dogma that hypertension is primarily a consequence of hemodynamic alterations has changed over the recent past, with compelling evidence that high blood pressure is linked to vascular damage, oxidative stress and inflammation. Of the many factors implicated in hypertensive vascular disease, angiotensin II appears to be one of the most important. Angiotensin II, a multifunctional peptide regulating vascular contraction, growth and fibrosis, has recently been identified as proinflammatory mediator. Angiotensin II increases vascular permeability, promotes recruitment of inflammatory cells into tissues, and directly activates infiltrating immune cells, which further contribute to the inflammatory process. Moreover, angiotensin II participates in tissue repair and remodeling, by stimulating cell growth and fibrosis. Many of these processes are mediated through increased generation of reactive oxygen species (oxidative stress). Summary Inflammation, oxidative stress and hypertension are closely interrelated. Here we discuss the (patho)physiology of vascular inflammation in hypertension, focusing specifically on the role of angiotensin II and reactive oxygen species. By understanding molecular and cellular mechanisms of hypertensive vascular disease will allow for more targeted therapy and hopefully improved management and treatment of patients with hypertension. Abbreviations CRP: C-reactive protein; ICAM: intercellular cell adhesion molecule; MAP: mitogen-activated protein; MCP-1: monocyte chemotactic protein-1; MMP: matrix metalloproteinase; NAD(P)H: nicotinamide adenine dinucleotide phosphate, reduced form; NF-κB: nuclear factor κB; NOS: nitric oxide synthase; ROS: reactive oxygen species; TNF: tumor necrosis factor; VCAM: vascular cell adhesion molecule; VEGF: vascular endothelial cell growth factor; VSMC: vascular smooth muscle cell.
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Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.002 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.007 | 0.001 |
| Bibliometrics | 0.002 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.002 | 0.002 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it