ArticleMolecular & cellular proteomics : MCP2026
An Integrated Cardiac Microtissue Proteome Map Extends Therapeutic Remodeling by Nanovesicles.
Article in Molecular & cellular proteomics : MCP, 2026. 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human cardiac microtissues are a promising model to study cardiac biology and disease, but their application is constrained by therapeutic remodeling strategies and limited knowledge of their functional protein expression profiles. Here, we define the use of human cardiac microtissue (hCMT) model generated by assembling induced pluripotent stem cell-derived endothelial cells, cardiac fibroblasts, and cardiomyocytes (CMs) to model ischemia-reperfusion injury (IRI) through a model of hypoxia and reoxygenation and nanovesicle (NV)-mediated functional remodeling. Engineered NVs, generated directly from human stem cells, have been shown to influence cardiac tissue and cell repair, and provide a platform for scalable and reproducible cell free-mediated therapy. We show the functional regulation of the hCMT model and define that administration of NVs (from human induced pluripotent stem cell origin) during reoxygenation significantly increase CM survival and preserve contractility function (contractile duration, relaxation time, and relaxation:contraction velocity). We establish NV uptake and transfer with target cells from the hCMT model. Quantitative proteomics was applied to decipher the cell proteome dynamics and molecular mechanisms of IRI in our in vitro model following NV treatment, linked with networks associated with cell survival, energy production, and stress response regulation. Notably, cell type-specific enrichment analysis revealed that NVs drive distinct proteomic remodeling based on their cell origin, where CERA NVs selectively upregulate cytoprotective and structural networks (such as HSP70, MYH6, and XIRP1) within parenchymal CMs, whereas CL2 NVs predominantly suppress non-myocyte activation and extracellular matrix remodeling factors within the endothelial and fibroblast compartments. Our findings provide an advanced human stem cell-based platform to understand underlying mechanisms of IRI and assess cell-free therapeutic cardioprotective strategies.
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.