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Record W7126350943

From biomarker to therapeutic target : the role of myo-inositol and SMIT1 in heart failure and cardiac fibrosis

2025· dissertation· en· W7126350943 on OpenAlexaboutno aff
Julien Cumps

Bibliographic record

VenueDigital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) · 2025
Typedissertation
Languageen
FieldMedicine
TopicCardiovascular Function and Risk Factors
Canadian institutionsnot available
Fundersnot available
KeywordsHeart failureCardiac fibrosisBiomarkerMyofibroblastPathogenesisMyocardial infarctionDownregulation and upregulationMyocardial fibrosisExtracellular matrix
DOInot available

Abstract

fetched live from OpenAlex

Heart failure (HF) is a complex syndrome in which metabolic disturbances contribute significantly to disease progression. Among these, the cyclic polyol myo-inositol has recently emerged as a metabolite of interest. Transported into the heart by the sodium/myo-inositol transporter 1 (SMIT1), myo-inositol has been implicated in oxidative stress and maladaptive remodelling, yet its clinical and mechanistic relevance in heart failure has not been fully defined. In two large patient cohorts from Belgium and Canada, plasma myo-inositol concentrations were consistently higher in patients with HF than in controls, with the highest levels observed in HFpEF. In this subgroup it was independently associated with impaired renal function, poor clinical outcomes, and structural remodelling markers, particularly fibrotic. These observations suggest that circulating myo-inositol might not only be a biomarker but also a potential contributor to the pathogenesis of HFpEF. Mechanistic studies support this hypothesis. In vitro, exposure of human cardiac fibroblasts to myo-inositol stimulated proliferation, migration, and differentiation into contractile myofibroblasts, thereby enhancing extracellular matrix production. In HFrEF human hearts, SMIT1 expression was markedly increased in fibrotic regions, and transcriptomic analyses linked its upregulation to pro-fibrotic signaling networks. Consistently, mouse models of myocardial infarction demonstrated increased SMIT1 expression in areas of fibrosis. Moreover, cardiac fibroblasts derived from SMIT1-deficient mice showed blunted responses to TGF-β, with reduced myofibroblast differentiation, contractility, and collagen deposition. Taken together, these findings identify the myo-inositol/SMIT1 axis as a key driver of fibroblast activation and myocardial fibrosis. Elevated plasma myo-inositol provides prognostic information in HF, particularly HFpEF, while SMIT1-mediated transport enables the cellular processes that underlie adverse remodelling. This integrative evidence highlights the myo-inositol/SMIT1 pathway as both a marker of disease severity and a potential therapeutic target to mitigate fibrosis and improve outcomes in HF.

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)0.003
metaresearch head score (Gemma)0.003
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Not applicable · Consensus signal: none
GenreCandidate signal: Other · Consensus signal: none
Teacher disagreement score0.004
Threshold uncertainty score0.013

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0030.003
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0020.001
Bibliometrics0.0010.001
Science and technology studies0.0000.001
Scholarly communication0.0040.002
Open science0.0010.001
Research integrity0.0020.005
Insufficient payload (model declined to judge)0.0030.001

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 head0.007
GPT teacher head0.207
Teacher spread0.200 · 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 designNot applicable
Domainnot available
GenreOther

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

Explore more

Same venueDigital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B))Same topicCardiovascular Function and Risk FactorsFrench-language works237,207