Mechanisms for the development of heart failure and improvement of cardiac function by angiotensin-converting enzyme inhibitors
Bibliographic record
Abstract
Angiotensin-converting enzyme (ACE) inhibitors, which prevent the conversion of angiotensin I to angiotensin II, are well-known for the treatments of cardiovascular diseases, such as heart failure, hypertension and acute coronary syndrome. Several of these inhibitors including captopril, enalapril, ramipril, zofenopril and imidapril attenuate vasoconstriction, cardiac hypertrophy and adverse cardiac remodeling, improve clinical outcomes in patients with cardiac dysfunction and decrease mortality. Extensive experimental and clinical research over the past 35 years has revealed that the beneficial effects of ACE inhibitors in heart failure are associated with full or partial prevention of adverse cardiac remodeling. Since cardiac function is mainly determined by coordinated activities of different subcellular organelles, including sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils, for regulating the intracellular concentration of Ca2+ and myocardial metabolism, there is ample evidence to suggest that adverse cardiac remodelling and cardiac dysfunction in the failing heart are the consequence of subcellular defects. In fact, the improvement of cardiac function by different ACE inhibitors has been demonstrated to be related to the attenuation of abnormalities in subcellular organelles for Ca2+-handling, metabolic alterations, signal transduction defects and gene expression changes in failing cardiomyocytes. Various ACE inhibitors have also been shown to delay the progression of heart failure by reducing the formation of angiotensin II, the development of oxidative stress, the level of inflammatory cytokines and the occurrence of subcellular defects. These observations support the view that ACE inhibitors improve cardiac function in the failing heart by multiple mechanisms including the reduction of oxidative stress, myocardial inflammation and Ca2+-handling abnormalities in cardiomyocytes.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot 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.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.001 | 0.002 |
| Scholarly communication | 0.002 | 0.001 |
| Open science | 0.002 | 0.001 |
| Research integrity | 0.002 | 0.003 |
| Insufficient payload (model declined to judge) | 0.007 | 0.002 |
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 source (direct Gemma or distilled Codex), 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".