ArticleProteomics2026
A Single-Cell Proteomic Atlas of Cardiac Fibrosis Reveals Cell-Type-Specific Remodeling and Discordant Protein Regulation.
Article in Proteomics, 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
7 authors.
Funding
Abstract
Cardiac fibrosis is a hallmark of progressive cardiac remodeling and heart failure, characterized by excessive extracellular matrix (ECM) deposition and complex cellular interactions. While bulk proteomic studies have provided insights into global protein alterations associated with fibrosis, they inherently average signals across heterogeneous cardiac cell populations, limiting resolution of cell-type-specific protein regulation. In this study, we applied single-cell proteomics by mass spectrometry (SCoPE2) to generate a proteomic atlas of cardiac fibrosis in an isoproterenol-induced mouse model. Across 1,163 high-quality single cells (ISO: 581; Control: 582), we quantified 4,251 proteins and resolved five major cardiac cell populations, including cardiomyocytes, endothelial cells, fibroblasts, M2 macrophage-like cells, and smooth muscle cells. Single-cell analysis revealed extensive cell-type-specific and discordant protein regulation that was largely masked in bulk proteomic measurements. These fundings demonstrate the utility of single-cell proteomics for resolving cellular heterogeneity in fibrotic cardiac tissue and provide a resource for future integrative studies of cardiac remodeling.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.