ArticleNature communications2021
Alteration of circadian machinery in monocytes underlies chronic kidney disease-associated cardiac inflammation and fibrosis.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 78 citations in OpenAlex.
- Unveiling the impact of colonic pH and pH-sensing receptors in blood pressure regulation.Gut microbes · 2026Review
- Circadian mechanisms in heart failure: Cell-specific regulation and chrono-medicine.Cell insight · 2026Review
- Effects of chronic jetlag on high-fat and high-fructose diet induced renal injury in mice.Scientific reports · 2026Article
- Targeting Circadian Rhythm Disruption in Glaucoma: PTGDS Mediates Trabecular Meshwork Fibrosis and Is Therapeutically Targeted by Aprepitant.Translational vision science & technology · 2026Article
- Therapeutic Strategies Targeting the Kidney-Liver-Immune-Heart Network: Circadian and Mechanosensory Pathways in CKD-Associated Cardiac Injury.International journal of molecular sciences · 2026Review
- The Interplay Between Circadian Clocks and the Tumour Microenvironment in Breast Cancer.Cancers · 2026Review
- Diastolic Blood Pressure Variability Predicts Cardiovascular Outcomes in CKD, Especially in Advanced Stages.Kidney medicine · 2026Article
- Hericenone C exhibits anti-nociceptive effects through RORα-mediated suppression of TLR4 transcription.Frontiers in pharmacology · 2026Article
- Research Progress of BMAL1 in Heart Failure.Journal of the American Heart Association · 2025Review
- Bovine milk exosomes influence transcriptome profiles and reduce cardiac fibrosis in a rat model.Scientific reports · 2025Article
- Time to Reset: The Interplay Between Circadian Rhythms and Redox Homeostasis in Skeletal Muscle Ageing and Systemic Health.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidative Stress Triggers Porcine Ovarian Granulosa Cell Apoptosis Through MAPK Signaling.Antioxidants (Basel, Switzerland) · 2025Article
- Inflammatory and Cardiovascular Events in CKD: The Multi-Ethnic Study of Atherosclerosis (MESA).American journal of kidney diseases : the official journal of the National Kidney Foundation · 2025Observational
- Circadian Gene NPAS2 Relieves Hypertrophic Scar Formation via CDC25A-Mediated Fibroblasts Activity.Journal of cellular and molecular medicine · 2025Article
- BMAL1 Regulates Collagen Production in the Myometrium and Leiomyomas.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Acid sensing to inflammaging: mechanisms and therapeutic promise of GPR68 (OGR1) in aging-related diseases.Frontiers in aging · 2025Review
- Targeting macrophage circadian rhythms with microcurrent stimulation to activate cancer immunity through phagocytic defense.Theranostics · 2025Article
- Chronotherapy and intervertebral disc degeneration: understanding the role of circadian rhythm in degenerative processes.Frontiers in cell and developmental biology · 2025Review
- GPR68 Mediates Lung Endothelial Dysfunction Caused by Bacterial Inflammation and Tissue Acidification.Cells · 2024Article
- Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment.International journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunction of the circadian clock has been implicated in the pathogenesis of cardiovascular disease. The CLOCK protein is a core molecular component of the circadian oscillator, so that mice with a mutated Clock gene (Clk/Clk) exhibit abnormal rhythms in numerous physiological processes. However, here we report that chronic kidney disease (CKD)-induced cardiac inflammation and fibrosis are attenuated in Clk/Clk mice even though they have high blood pressure and increased serum angiotensin II levels. A search for the underlying cause of the attenuation of heart disorder in Clk/Clk mice with 5/6 nephrectomy (5/6Nx) led to identification of the monocytic expression of G protein-coupled receptor 68 (GPR68) as a risk factor of CKD-induced inflammation and fibrosis of heart. 5/6Nx induces the expression of GPR68 in circulating monocytes via altered CLOCK activation by increasing serum levels of retinol and its binding protein (RBP4). The high-GPR68-expressing monocytes have increased potential for producing inflammatory cytokines, and their cardiac infiltration under CKD conditions exacerbates inflammation and fibrosis of heart. Serum retinol and RBP4 levels in CKD patients are also sufficient to induce the expression of GPR68 in human monocytes. Our present study reveals an uncovered role of monocytic clock genes in CKD-induced heart failure.
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.