ArticleArteriosclerosis, thrombosis, and vascular biology2026
Endothelial Nucleoporin93 (Nup93) Maintains Vascular Homeostasis via Sun1-Dependent Regulation of RhoA/ROCK Activity.
Article in Arteriosclerosis, thrombosis, and vascular biology, 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.
- Mechanoresponsive modulation of nuclear pore complex structure and function bybioRxiv : the preprint server for biology · 2026Article
Corrections and comments
- Update of
Authors and funding
15 authors.
Funding
Abstract
backgroundAs the innermost lining of blood vessels, endothelial cells regulate barrier function, maintain vascular tone, and limit inflammation for vessel health. Involved in various fundamental endothelial processes, RhoA (Ras homolog family member A)/ROCK (Rho-associated coiled-coil containing protein kinase) signaling has been identified as a major contributor to age-associated hypertension and vascular disease; RhoA/ROCK hyperactivation promotes vessel permeability and impairs nitric oxide (NO) production. Recent studies identify Sun1 (Sad1 and UNC84 [protein UNC-84 homolog A] domain-containing protein 1), a key component of the linker of nucleoskeleton and cytoskeleton complex, as a major repressor of RhoA/ROCK activity. Our latest studies identify endothelial loss of Nup93 (nucleoporin93), a component of the nuclear pore complex, as a hallmark of vascular aging. Insinuating a role for nuclear envelope components in vessel homeostasis, the role of Nup93 in RhoA/ROCK signal regulation, however, remains entirely unknown.
methodsTargeted Nup93 knockdown approaches were used in primary human endothelial cells to assess the role of Nup93 in endothelial RhoA/ROCK signaling and downstream readouts, including endothelial barrier function, cellular stiffness, and eNOS (endothelial NO synthase) function. Rescue studies include the use of pharmacological ROCK inhibitors and lentiviral-mediated Sun1 restoration methods. We additionally measure barrier function and vessel reactivity in our novel inducible endothelial-specific Nup93 mouse model.
resultsTargeted loss of endothelial Nup93 significantly increases RhoA/ROCK activity for consequent endothelial permeability and decreased NO bioavailability both in vitro and in vivo. Mechanistically, we find that loss of Nup93 drastically reduces endothelial Sun1 levels for a concomitant increase in RhoA activity. Indeed, restoring Sun1 protein levels in Nup93-deficient endothelial cells mitigates RhoA activity, thereby rescuing both endothelial barrier function and eNOS expression.
conclusionsTaken together, we demonstrate endothelial Nup93 as a novel regulator of vascular permeability and NO-dependent vessel reactivity, contributing to the growing importance of nuclear membrane components in endothelial cell and vascular biology.
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.