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Record W4415262857 · doi:10.1161/hyp.82.suppl_1.th152

Abstract TH152: Molecular Pathways of Cardiac Fibrosis in Hypertension: A Systematic Review of Mechanisms and Therapeutic Implications

2025· article· en· W4415262857 on OpenAlexaboutno aff
Zaraq Khan, Inshal Jawed, Maqbool Qadir, Umme Farwa

Bibliographic record

VenueHypertension · 2025
Typearticle
Languageen
FieldMedicine
TopicHormonal Regulation and Hypertension
Canadian institutionsnot available
Fundersnot available
KeywordsFibrosisMyocardial fibrosisObservational studyBlood pressureCardiac fibrosisHeart failureAngiotensin IIRandomized controlled trial

Abstract

fetched live from OpenAlex

Introduction: Heart fibrosis caused by high blood pressure is the main reason behind heart failure and stiffness. Excessive activation of RAAS, TGF-β, and ongoing inflammation are examples of molecular changes related to the development of myocardial fibrosis in high blood pressure conditions. The significance of these pathways and their possible use as drug targets has not been investigated broadly. Our goal was to assemble information about the mechanisms of cardiac fibrosis in hypertension and to determine how treatment might affect them. Hypothesis: Using combination therapy that targets RAAS along with TGF-β will lead to a greater decrease in myocardial fibrosis and help improve diastolic function than standard RAAS blockade alone in patients with hypertension and elevated TGF-β, galectin-3 and procollagen type I C-terminal propeptide levels over 12 months. Methods: Following PRISMA guidelines, we reviewed studies looking at molecular indicators or processes of myocardial fibrosis in patients with hypertension. Studies were included: 3 randomized controlled trials and 12 observational studies. These studies examined markers in the blood and heart, how the heart tissue appeared on imaging, and whether fibrosis affected the outcomes. The ability to identify errors was reviewed through the Cochrane Risk of Bias for randomized controlled trials and the Newcastle-Ottawa for observational studies. Results: Patients with hypertension tend to have higher levels of profibrotic mediators such as angiotensin II, aldosterone, TGF-β, and inflammatory cytokines. Observational studies suggest a clear link between high levels of circulating fibrosis markers and both the increased thickness of the left ventricle and reduced heart-filling ability in hypertensive people. In small RCTs, RAAS blockade with ACE inhibitors, ARBs, or mineralocorticoid receptor antagonists helped lower fibrosis biomarkers. It could even restore some of the fibrotic changes seen in the heart. The chance of bias was very low in RCTs, compared to observational studies. Conclusions: Several pathways working together contribute to myocardial fibrosis in hypertension, and changing their roles can help prevent heart damage. It emphasizes that besides reducing blood pressure, using approaches to prevent fibrosis may bring more cardiovascular benefits. More studies are needed to find and develop customized antifibrotic therapies for hypertensive heart disease.

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 machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.015
metaresearch head score (Gemma)0.037
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Systematic review · Consensus signal: Systematic review
GenreCandidate signal: Review · Consensus signal: Review
Teacher disagreement score0.015
Threshold uncertainty score0.077

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0150.037
Meta-epidemiology (narrow)0.0020.001
Meta-epidemiology (broad)0.0080.010
Bibliometrics0.0120.012
Science and technology studies0.0010.001
Scholarly communication0.0020.002
Open science0.0020.002
Research integrity0.0020.001
Insufficient payload (model declined to judge)0.0070.000

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.

Opus teacher head0.028
GPT teacher head0.262
Teacher spread0.234 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designSystematic review
Domainnot available
GenreReview

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".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

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