Bibliographic record
Abstract
PURPOSE OF REVIEW: Transmission of external signals from the cell surface to the internal cellular environment occurs via tightly controlled complex transduction pathways. Alterations in these highly regulated signalling cascades in vascular smooth cells may play a fundamental role in the structural, mechanical and functional abnormalities that underlie vascular pathological processes in hypertension. The present review focuses on recent developments relating to two novel signalling pathways: angiotensin II signalling through tyrosine kinases; and oxidative stress and redox-dependent signal transduction. These pathways are emerging as critical mediators of hypertensive vascular disease because they influence multiple cellular responses that are involved in structural remodelling, vascular inflammation and altered tone. RECENT FINDINGS: A recent advance in the field of angiotensin II signalling was the demonstration that, in addition to its vasoconstrictor properties, angiotensin II has potent mitogenic-like and proinflammatory-like characteristics. These actions are mediated through phosphorylation of both nonreceptor tyrosine kinases and receptor tyrosine kinases. It is also becoming increasingly apparent that many signalling events that underlie abnormal vascular function in hypertension are influenced by changes in intracellular redox status. In particular, increased bioavailability of reactive oxygen species (oxidative stress) stimulates growth-signalling pathways, induces expression of proinflammatory genes, alters contraction-excitation coupling and impairs endothelial function. SUMMARY: A better understanding of the molecular pathways that regulate vascular smooth muscle cell function will provide further insights into the pathophysiological mechanisms that contribute to vascular changes and end-organ damage associated with high blood pressure, and could permit identification of potential novel therapeutic targets in the prevention and management of hypertension.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
How this classification was reachedexpand
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 | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.006 | 0.001 |
| Bibliometrics | 0.002 | 0.002 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 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 itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".