ArticleInternational journal of clinical and experimental pathology2018
Relationship between CaSRs and LPS-injured cardiomyocytes.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Research progress on cellular behavior of CaSR in cardiovascular diseases.Frontiers in immunology · 2025Review
- Alcohol Intake Provoked Cardiomyocyte Apoptosis Via Activating Calcium-Sensing Receptor and Increasing Endoplasmic Reticulum Stress and Cytosolic [Ca2+]i.Cell biochemistry and biophysics · 2023Article
- PKM2 deficiency exacerbates gram-negative sepsis-induced cardiomyopathy via disrupting cardiac calcium homeostasis.Cell death discovery · 2022Article
- Rosuvastatin exerts cardioprotective effect in lipopolysaccharide-mediated injury of cardiomyocytes in an MG53-dependent manner.BMC cardiovascular disorders · 2022Article
- Calcium-Sensing Receptor (CaSR), Its Impact on Inflammation and the Consequences on Cardiovascular Health.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCalcium-sensing receptors (CaSRs) regulate systemic calcium homeostasis. Intracellular calcium concentration changes are initiating factors of endoplasmic reticulum stress and cell autophagy. Recent research has revealed that CaSRs play an important role in myocardial ischemia/reperfusion injury and other cardiovascular diseases. However, it remains unclear whether CaSRs are involved in lipopolysaccharide (LPS)-induced cardiomyocyte injury.
methodsCultured neonatal rat cardiomyocytes were treated with LPS, with or without pretreatment by a CaSR specific agonist SC-211006 or CaSR specific antagonist SC-207394. The ultrastructure of cardiomyocytes was observed using a transmission electron microscope, and the expression of CaSR, GRP78, LC3B, CytC and Bcl-2 proteins were detected by western blot.
resultsCompared with the control group, LPS increased cardiomyocyte injury and the expression of CaSR, GRP78, LC3B and CytC proteins, but decreased the expression of Bcl-2. Compared with the LPS group, pretreatment with SC-211006 further enhanced cardiomyocyte damage and the expression of CaSR, GRP78, LC3B and CytC, but reduced the expression of Bcl-2. Conversely, pretreatment with SC-207394 decreased cardiomyocyte injury and the protein expression of CaSR, GRP78, LC3B and CytC, but increased the expression of Bcl-2.
conclusionOur results suggest that CaSRs are involved in LPS-induced rat cardiomyocyte injury via the activation of endoplasmic reticulum stress and autophagy.
Indexed as
Identifiers
31938302PMC6958229W3027762319What 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.