ArticleJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology2023
The microtubule signature in cardiac disease: etiology, disease stage, and age dependency.
Article in Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Paclitaxel-induced cytoskeletal and focal adhesion reorganisation alters connexin43 and α-smooth muscle actin in cardiac cells.In vitro cellular & developmental biology. Animal · 2026Article
- Phospho-mimic βIII-tubulin rescues microtubule and cardiac defects in Duchenne muscular dystrophy mice.Journal of molecular and cellular cardiology · 2026Article
- Tubulin Post-Translational Modifications in Cardiovascular Diseases: Emerging Mechanisms and Therapeutic Modulation by Traditional Chinese Medicine.Drug design, development and therapy · 2026Review
- Case Series: Genetic mimics of hypertrophic cardiomyopathy in elderly.Frontiers in cardiovascular medicine · 2025Article
- Microtubule destabilization with colchicine increases the work output of myocardial slices.Journal of molecular and cellular cardiology plus · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Employing animal models to study heart failure (HF) has become indispensable to discover and test novel therapies, but their translatability remains challenging. Although cytoskeletal alterations are linked to HF, the tubulin signature of common experimental models has been incompletely defined. Here, we assessed the tubulin signature in a large set of human cardiac samples and myocardium of animal models with cardiac remodeling caused by pressure overload, myocardial infarction or a gene defect. We studied levels of total, acetylated, and detyrosinated α-tubulin and desmin in cardiac tissue from hypertrophic (HCM) and dilated cardiomyopathy (DCM) patients with an idiopathic (n = 7), ischemic (n = 7) or genetic origin (n = 59), and in a pressure-overload concentric hypertrophic pig model (n = 32), pigs with a myocardial infarction (n = 28), mature pigs (n = 6), and mice (n = 15) carrying the HCM-associated MYBPC3
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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 OpenQuestion graph.