ArticleCardiovascular research2026
Identification of unannotated microproteins involved in endothelial cell homeostasis, dysfunction, and vascular disease.
Article in Cardiovascular research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A microprotein encoded by FERMT3 modulates endothelial cell protein catabolism and induces cell cycle arrest and senescence.Cell communication and signaling : CCS · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
aimsMicroproteins (miPs) translated from small open reading frames (smORFs) are crucial regulators of cell function. However, the expression and function of miPs in endothelial cells and alterations in miP expression linked with inflammation and cardiovascular disease, remain largely unexplored. METHODS AND
resultsAn optimized proteogenomic approach combining RiboTag RNA-sequencing and mass spectrometry of the small molecular mass proteome was utilized to identify endothelial cell-specific miPs. Heart, lung, and blood vessels from endothelial cell-specific RiboTag mice and human endothelial cells were studied under homeostatic and inflammatory conditions. We identified 2739 murine as well as 1365 intracellular and 607 extracellular human endothelial cell miPs encoded from previously non-canonical (unannotated) smORFs. Vascular inflammation induced in vitro by interleukin-1β (IL-1β) and in vivo through PCSK9 overexpression, high-fat diet, and partial carotid artery ligation significantly altered smORF expression. An additional 347 miPs were detected in human serum, 23 decreasing and 31 increasing, after cardiac damage. The expression of an inflammation-induced miP encoded by an internal smORF within the proline-serine-threonine phosphatase interacting protein 2 (PSTPIP2) transcript, that is, miP-PSTPIP2, was assessed using a custom antibody. miP-PSTPIP2 expression was upregulated in IL-1β-treated human endothelial cells, in pre-atherosclerotic murine carotid arteries and detected in carotid arteries from patients with atherosclerosis. The relevance of 250 miPs for endothelial cell growth and viability was demonstrated using a high-throughput clustered regularly interspaced Short palindromic Repeats (CRISPR)/Cas9 screen.
conclusionTaken together, we document the existence of a large number of human and murine miPs encoded by non-canonical smORFs and their altered expression in inflammatory conditions. The identification of secreted miPs suggests that they may also exert autocrine or paracrine functions. These novel small peptides modulate cell proliferation and survival in endothelial cells and may play a significant role in human cardiovascular disease.
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.