Background: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is recognized as an independent risk factor of cardiovascular disease. The release of Ca2+ mediated by transient receptor potential canonical (TRPC) channels participates in the hypoxia-induced pathophysiological changes in the cardiovascular systems in case of OSAHS. This study aimed to investigate which subtypes of TRPCs were involved in OSAHS in a rat model of intermittent hypoxia.

Methods: OSAHS was induced by exposure of rats to intermittent hypoxia. The expression of TRPCrelated genes and proteins in the cardiomyocytes by qRT-PCR and Western Blotting, respectively.

Results: The mRNA expression of TRPC3/TRPC4/TRPC5 increased significantly in OSAHS group compared with the control group (P<0.05). The TRPC5 protein expression was significantly higher in the OSAHS control than the control group (P<0.05).

Conclusions: The TRPC5 channel is likely to be involved in the OSAHS induced pathophysiological changes in the myocardium and may become a target to prevent OSAHS related cardiac damage.

Download full-text PDF

Source
http://dx.doi.org/10.21037/apm.2020.04.08DOI Listing

Publication Analysis

Top Keywords

transient receptor
8
receptor potential
8
potential canonical
8
obstructive sleep
8
sleep apnea-hypopnea
8
apnea-hypopnea syndrome
8
osahs
5
canonical channel
4
channel involved
4
involved cardiac
4

Similar Publications

Ethnopharmacological Relevance: Acute ischemic stroke (AIS) is an important cause of death and disability in the world. Based on the blood stasis syndrome of stroke, Shuxuetong Injection (SXT) is a representative prescription for the treatment of AIS, which extracted by modern technology from Whitmania pigra Whitman (Shuizhi) and Pheretima aspergillum E.Perrier (Dilong).

View Article and Find Full Text PDF

Systematic review of Neuropsychiatric Toxicity in Second Generation Antifungals with an illustrative Case Reports.

J Acad Consult Liaison Psychiatry

March 2025

Hospices Civils de Lyon, Hôpital Louis Pradel, service de Psychiatrie de liaison, F-69000 Lyon, France.

Background: Second generation triazole antifungals are extended-spectrum drugs that act against yeasts, molds, and dimorphic fungi. These agents include voriconazole, posaconazole, and isavuconazole. Voriconazole may cause neuropsychiatric toxicity such as hallucinations.

View Article and Find Full Text PDF

There are indications that the transient blockade of the dopamine receptor D2 (DRD2) by atypical antipsychotics such as risperidone is related to their metabolic side effects. We, therefore, examined the relationship between TaqIA polymorphism of the DRD2 gene and acute risperidone-induced metabolic changes. We recruited 153 newly diagnosed patients with psychotic disorders (71 males and 82 females) from the Federal Neuropsychiatric Hospital, Yaba, Lagos, Nigeria.

View Article and Find Full Text PDF

The CD2-depleting drug alefacept (LFA3-Ig) preserved beta cell function in new-onset type 1 diabetes (T1D) patients. The most promising biomarkers of response were late expansion of exhausted CD8 T cells and rare baseline inflammatory islet-reactive CD4 T cells, neither of which can be used to measure responses to drug in the weeks after treatment. Thus, we investigated whether early changes in T cell immunophenotypes could serve as biomarkers of drug activity.

View Article and Find Full Text PDF

Decoy receptor 3 (DcR3), a soluble receptor in the tumor necrosis factor receptor superfamily, regulates the functions of monocytes, macrophages, dendritic cells, and T cells. Previous studies have demonstrated that DcR3 suppresses B cell proliferation in vitro and ameliorates autoimmune diseases in animal models; however, whether and how DcR3 regulates antibody production is unclear. Using a DcR3 transgenic mouse model, we found that DcR3 impaired the T cell-dependent antigen-stimulated antibody response.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!