ArticleRespiratory research2026
Activation of α7nAChR prevents maladaptive right ventricular remodeling via inhibiting the recruitment of CCR2
Article in Respiratory 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
Abstract
backgroundThe transition from adaptive to maladaptive right ventricular (RV) remodeling leads to RV failure (RVF), which is the strongest predictor of mortality in pulmonary arterial hypertension (PAH). However, effective treatments for PAH RVF are currently lacking. Recent studies have implicated C–C chemokine receptor type 2 (CCR2)+ macrophages in promoting PAH RVF. Stimulation of α7 nicotinic acetylcholine receptors (α7nAChR) expressed on macrophages regulates local and systemic inflammation. This study aimed to evaluate the effects of α7nAChR activation on RV remodeling and inflammation in PAH.
methodsMonocrotaline (MCT)-induced PAH rats were used to mimic the continuum of RV remodeling. The dynamics of RV CCR2+ macrophages, CD43lowHis48high monocytes and inflammatory genes expression were investigated by immunostaining, flow cytometry and real-time polymerase chain reaction. MCT rats were treated with the selective α7nAChR agonist PNU-282987 or the antagonist methyllycaconitine consecutively for 4 weeks, starting 1 week after MCT injection. Echocardiography, hemodynamics and RV pathology were assessed. The abundance, functional phenotype and C–C chemokine ligand 2 (CCL2) secretion of RV CCR2+ macrophages were evaluated. In vitro activation of α7nAChR was performed on bone-marrow derived macrophages.
resultsIncreased infiltration of RV CCR2+ macrophages and CD43lowHis48high monocytes, and elevated inflammatory gene expression were associated with maladaptive RV remodeling in PAH rats. In vivo, PNU-282987 reduced mortality, prevented maladaptive RV remodeling, and restored RV function. Furthermore, PNU-282987 inhibited the recruitment of RV CCR2+ macrophages by suppressing the CCL2-CCR2 chemotactic axis and enhanced the anti-inflammatory phenotype of RV CCR2+ macrophages. In vitro experiments confirmed these effects of PNU-282987 on CCR2+ macrophages.
conclusionActivation of α7nAChR prevents PAH-induced maladaptive RV remodeling by inhibiting the recruitment of CCR2+ macrophages, thereby offering a novel therapeutic strategy for PAH RVF.
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.