ArticleFrontiers in cardiovascular medicine2025
A pathogenic titin missense mutation in hiPSC-derived cardiomyocytes predisposes to ventricular fibrillation in acute ST-segment elevation myocardial infarction.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: There is growing evidence that genetic factors may play a crucial role in the development of ventricular fibrillation (VF) following acute ST-segment elevation myocardial infarction (STEMI). Previous studies have demonstrated that both truncating and missense mutations in the TTN gene, which encodes a large cellular structural protein, are linked to arrhythmogenesis. However, the precise role of TTN mutations in the onset of primary VF after acute STEMI remains poorly understood. Objectives: The primary objective of this study was to comprehensively determine the role and elucidate the electrophysiological mechanism of TTN missense mutations in VF development after acute STEMI. This was achieved by leveraging the unique capabilities of human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Methods: Whole-genome sequencing identified TTN mutations in four out of six unrelated patients who experienced VF after STEMI (STEMI/VF). Induced pluripotent stem cells were successfully generated from the peripheral blood mononuclear cells obtained from a 47-year-old male carrying a novel TTN variant (c.43803T>A/p.D14601E) and from an unrelated healthy control. Subsequently, a directed differentiation protocol was employed to create iPSC-CMs, followed by rigorous electrophysiological and functional analyses to elucidate the mechanisms underlying the observed phenotypes. Results: Compared with the control iPSC-CMs, the patient-derived iPSC-CMs with STEMI/VF exhibited a significant shortening of the action potential duration (APD). Specifically, peak sodium channel current (I Conclusions: The iPSC-CMs obtained from the patient carrying a TTN missense mutation and who suffered from VF after STEMI exhibited a decrease in I
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.