ArticleJournal of molecular and cellular cardiology2016
Deletion of calponin 2 in macrophages alters cytoskeleton-based functions and attenuates the development of atherosclerosis.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 26 citations in OpenAlex.
- Genetic evidence and cross-species functional characterization implicateProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers.Scientific reports · 2026Article
- PRSS23 functions downstream of ZEB1 to promote esophageal squamous cell carcinoma progression by driving M2 polarization of tumor associated macrophages.Molecular and cellular biochemistry · 2026Article
- Galactomyces ferment filtrate upregulates anchoring junctions and stabilizes actin to maintain the Young's modulus of skin cells in vitro.International journal of cosmetic science · 2026Article
- Exploring potential diagnostic markers and therapeutic targets for type 2 diabetes mellitus with major depressive disorder through bioinformatics and in vivo experiments.Scientific reports · 2025Article
- Determination of selected oxysterol levels, oxidative stress, and macrophage activation indicators in children and adolescents with familial hypercholesterolemia.Lipids in health and disease · 2024Article
- Histone deacetylase inhibition enhances extracellular vesicles from muscle to promote osteogenesis via miR-873-3p.Signal transduction and targeted therapy · 2024Article
- Mechanoregulation and function of calponin and transgelin.Biophysics reviews · 2024Review
- Identification of hub genes and transcription factors in patients with primary gout complicated with atherosclerosis.Scientific reports · 2024Article
- Calponin 2 regulates ketogenesis to mitigate acute kidney injury.JCI insight · 2023Article
- Modulation of Smooth Muscle Cell Phenotype for Translation of Tissue-Engineered Vascular Grafts.Tissue engineering. Part B, Reviews · 2023Review
- Article
- Evolution and function of calponin and transgelin.Frontiers in cell and developmental biology · 2023Review
- Potential prognostic and immunotherapeutic value of calponin 1: A pan-cancer analysis.Frontiers in pharmacology · 2023Article
- Targeting the cytoskeleton and extracellular matrix in cardiovascular disease drug discovery.Expert opinion on drug discovery · 2022Review
- A rapid degradation of calponin 2 is required for cytokinesis.American journal of physiology. Cell physiology · 2021Article
- Sex as a Biological Variable in Atherosclerosis.Circulation research · 2020Review
- The Absence of Calponin 2 in Rabbits Suggests Caution in Choosing Animal Models.Frontiers in bioengineering and biotechnology · 2020Article
- Modulating Neuro-Immune-Induced Macrophage Polarization With Topiramate Attenuates Experimental Abdominal Aortic Aneurysm.Frontiers in pharmacology · 2020Article
- Downregulation of calponin 2 contributes to the quiescence of lung macrophages.American journal of physiology. Cell physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Arterial atherosclerosis is an inflammatory disease. Macrophages play a major role in the pathogenesis and progression of atherosclerotic lesions. Modulation of macrophage function is a therapeutic target for the treatment of atherosclerosis. Calponin is an actin-filament-associated regulatory protein that inhibits the activity of myosin-ATPase and dynamics of the actin cytoskeleton. Encoded by the gene Cnn2, calponin isoform 2 is expressed at significant levels in macrophages. Deletion of calponin 2 increases macrophage migration and phagocytosis. In the present study, we investigated the effect of deletion of calponin 2 in macrophages on the pathogenesis and development of atherosclerosis. The results showed that macrophages isolated from Cnn2 knockout mice ingested a similar level of acetylated low-density lipoprotein (LDL) to that of wild type (WT) macrophages but the resulting foam cells had significantly less hindered velocity of migration. Systemic or myeloid cell-specific Cnn2 knockouts effectively attenuated the development of arterial atherosclerosis lesions with less macrophage infiltration in apolipoprotein E knockout mice. Consistently, calponin 2-null macrophages produced less pro-inflammatory cytokines than that of WT macrophages, and the up-regulation of pro-inflammatory cytokines in foam cells was also attenuated by the deletion of calponin 2. Calponin 2-null macrophages and foam cells have significantly weakened cell adhesion, indicating a role of cytoskeleton regulation in macrophage functions and inflammatory responses, and a novel therapeutic target for the treatment of arterial atherosclerosis.
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.