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The Effect of Losartan on Marfan Syndrome Is Angiotensin II Receptor Type 1 (ATR1) Independent

2016· article· en· W2987698627 on OpenAlexafffundabout
Stephanie Sellers, Rayleigh Chan, Michael Mielnik, Una Jermilova, Marijana Pavlović, Jeremy A. Hirota, Michael A. Seidman, James C. Hogg, Pascal Bernatchez

Bibliographic record

VenueThe FASEB Journal · 2016
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicConnective tissue disorders research
Canadian institutionsChild and Family Research InstituteUniversity of British ColumbiaSt. Paul's Hospital
FundersCanadian Institutes of Health ResearchUniversity of British Columbia
KeywordsLosartanAngiotensin IIInternal medicineAngiotensin II receptor type 1EndocrinologyMedicineCardiologyReceptor

Abstract

fetched live from OpenAlex

Background Marfan Syndrome (MFS) leads to life threatening cardiovascular and pulmonary complications including aortic root dilation and emphysema‐like lung destruction. The new drug of choice to treat MFS is Losartan as it has been shown to reduce aortic and lung pathology in mouse models of MFS and is the focus of on‐going clinical trials. Losartan selectively blocks angiotensin receptor type I (ATR1), which is a key player in MFS pathogenesis. However, despite its promising therapeutic activity, Losartan has never been evaluated in the absences of its proposed target, and therefore genetic loss of ATR1 should protect against MFS and reveal the full potential of Losartan Hypothesis A model of MFS lacking ATR1 will prevent the cardiovascular and pulmonary phenotype of MFS and thereby confirm the mechanism of action of Losartan and reveal the full therapeutic potential of complete ATR1 blockade in MFS. Methods A MFS model lacking ATR1 was generated using a commonly used MFS model (Fibrillin C1039G) and ATR1 knockout mice (ATR1−/−). The resulting MFS ATR1−/− mice, both treated and untreated with Losartan, were used to evaluate the impact of ATR1 knockout on MFS. Aortic and lung pathology was evaluated through echocardiogram and histology while MFS skeletal manifestation were analyzed using radiography. Results Echocardiograms and histology show that both MFS and MFS ATR1−/− mice have similar aortic root dilation, aortic wall thickening and elastic fibre fragmentation in stark contrast to our hypothesis. Additionally, both MFS and MFS ATR1−/− groups demonstrate emphysema‐like airspace widening and significant changes in skeletal structure. Finally, when treated with Losartan MFS ATR1−/− mice showed similar reduction in aortic root dilation and airspace widening as MFS mice. Conclusion Data from our novel model shows that loss of the predominant ATR1 isoform fails to prevent MFS complications. Furthermore, Losartan treatment in the absence of ATR1 is still an effective therapeutic for MFS aortic and lung pathology. This suggests that the therapeutic utility of Losartan in MFS is off‐target and completely independent of ATR1. Support or Funding Information This work was supposed by funds from the Canadian Institutes of Health Research (CIHR) and fellowships to SS from CIHR and the University of British Columbia.

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 imitation

Not 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.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.013
Threshold uncertainty score0.254

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

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 head0.010
GPT teacher head0.271
Teacher spread0.261 · 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 teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

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".

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Citations0
Published2016
Admission routes3
Has abstractyes

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