ArticleThe Journal of international medical research2026
Homocysteine-induced endothelial dysfunction through mediating endoplasmic reticulum stress.
Article in The Journal of international medical research, 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
No grant is acknowledged in the PubMed record.
Abstract
ObjectiveEndothelial dysfunction is a key pathological process in cardiovascular and cerebrovascular diseases. Herein, we aimed to investigate the effect of homocysteine on endoplasmic reticulum stress in a model of endothelial dysfunction, focusing on glucose-regulated protein 78 mediation by homocysteine.MethodsWe established a hyperhomocysteinemia model in mice to examine the effect of homocysteine on cerebral microcirculation. In vitro, endothelial cells were used to explore the effect of homocysteine on endoplasmic reticulum stress. We conducted a bioinformatics study to investigate the impact of homocysteine on the vascular microenvironment. Furthermore, molecular dynamics simulation analysis was performed to explore the binding mode and stability between homocysteine and glucose-regulated protein 78.ResultsIn vivo, homocysteine increased the expression of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 in brain tissue, whereas reducing the expression of tight junction protein 1. Furthermore, inhibition of endoplasmic reticulum stress effectively improved endothelial dysfunction induced by homocysteine. Finally, molecular dynamics simulations revealed a critical interaction between homocysteine and glucose-regulated protein 78, which likely impacts binding affinity.ConclusionsHomocysteine causes cerebral microcirculatory disorders. The mechanism is related to homocysteine-induced endoplasmic reticulum stress through regulation of glucose-regulated protein 78 protein function.
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.