ArticleBasic research in cardiology2026
Activation of the C3a-C3aReceptor-axis is associated with endothelial dysfunction and glycocalyx damage in ST-elevation myocardial infarction.
Article in Basic research in cardiology, 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
8 authors.
Funding
Abstract
Complement activation is an early event in ischemia-reperfusion injury during ST-elevation myocardial infarction (STEMI) and drives endothelial dysfunction via glycocalyx (eGC) degradation. While downstream fragments such as C5a contribute to vascular injury, the role of the early anaphylatoxin C3a remains unclear. This study delineates the effects of the C3a:C3a-Receptor-axis on endothelial function, cytoskeletal dynamics, and eGC integrity. Sixty-four first-time STEMI patients and sixty-four age- and sex-matched healthy controls were enrolled. Patients were stratified into quartiles based on serum C3a concentrations, and comparisons were performed between the lowest vs. highest quartiles as well as between all STEMI patients vs. controls. Inflammatory and glycocalyx parameters were assessed via ELISA, AFM nanoindentation, and monocyte adhesion assays. NO bioavailability was measured chemiluminescence-based. C3a-receptor-antagonists (SB290157 and JR14a), C5a-Receptor1-antagonism (PMX53), as well as Rac1-Inhibition (NSC23766) were used to verify pathway specificity and downstream signaling involvement. High C3a levels were associated with marked endothelial injury: eGC height was reduced (- 44%; p < 0.001), cortical stiffness increased (+ 35%; p < 0.001), and shedding of Syndecan-1 and heparan sulfate was elevated (+ 203%, p < 0.001; + 181%, p < 0.01). NO bioavailability decreased by 34% (p < 0.05). C3a correlated inversely with eGC height (r = - 0.736) and positively with Syndecan-1 (r = 0.856). Treatment with recombinant C3a (250 ng/mL) induced cortical stiffening (+ 10.8%; p < 0.001), eGC loss (- 24.7%; p < 0.001), actin polymerization (+ 27.9%; p < 0.001), Rac1 activation (p < 0.05), reduced NO (- 38%; p < 0.05), and increased monocyte adhesion (+ 37%), all reversed by both C3a-Receptor-inhibitiors and by Rac1-inhibition. C3a:C3a-Receptor signaling drives Rac1-mediated cytoskeletal stiffening, eGC degradation, NO reduction, and leukocyte adhesion, promoting endothelial dysfunction in STEMI in both macrovascular and microvascular endothelial cells. This pathway represents a potential therapeutic target to mitigate complement-mediated vascular injury in acute myocardial infarction.
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.