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Ring finger protein 10 improves pirarubicin-induced cardiac inflammation by regulating the AP-1/Meox2 signaling pathway
Toxicol Appl Pharmacol. 2023 Feb 3:116411. doi: 10.1016/j.taap.2023.116411. Online ahead of print.ABSTRACTOBJECTIVES: Pirarubicin (THP) is widely used in clinical antitumor therapy, but its cardiotoxicity seriously affects the therapeutic effect in patients. In the study, we investigated the role of ring finger protein 10 (RNF10) in cardiotoxicity induced by THP.MATERIALS AND METHODS: A cardiac toxicity model in Sprague-Dawley (SD) rats induced by THP was established. Changes in diet, weight, electrocardiogram (ECG), and echocardiography were observed. Serum levels of brain natriuretic peptide (BNP), creatine kinase MB (CK...
Source: Toxicology and Applied Pharmacology - February 5, 2023 Category: Toxicology Authors: Liang Duan Heng Tang Ying Lan Hongwei Shi Peng Pu Quan He Source Type: research

PCSK9 Knockdown Can Improve Myocardial Ischemia/Reperfusion Injury by Inhibiting Autophagy
This study investigates the effect and mechanism of proprotein convertase subtilisin/Kexin type 9 (PCSK9) on myocardial ischemia-reperfusion injury (MIRI) and provides a reference for clinical prevention and treatment of acute myocardial infarction (AMI). We established a rat model of myocardial ischemia/reperfusion (I/R) and AC16 hypoxia/reoxygenation (H/R) model. A total of 48 adult 7-week-old male Sprague-Dawley rats were randomly assigned to three groups (n = 16): control, I/R, and I/R + SiRNA. In I/R and I/R + siRNA groups, myocardial ischemia was induced via occlusion of the left anterior descending branch (LAD) of t...
Source: Cardiovascular Toxicology - November 7, 2022 Category: Cardiology Authors: Guangwei Huang Xiyang Lu Zonggang Duan Kai Zhang Lei Xu Hailong Bao Xinlin Xiong Muzhi Lin Chao Li Yunquan Li Haiyan Zhou Zhenhua Luo Wei Li Source Type: research

TLR4-Myd88 pathway upregulated caveolin-1 expression contributes to coronary artery spasm
CONCLUSION: These findings suggested that Cav-1, which was upregulated by TLR4-Myd88, served as an important modulator of CAS microenvironment establishment in vivo and in vitro, making it a potential pharmacologic target for the treatment of vasospasm via reduced endothelial cell inflammation.PMID:34822994 | DOI:10.1016/j.vph.2021.106947
Source: Vascular Pharmacology - November 25, 2021 Category: Drugs & Pharmacology Authors: Xin Zhao Jinfan Tian Yue Liu Zhishuai Ye Mingyue Xu Rongchong Huang Xiantao Song Source Type: research

Canstatin modulates L-type calcium channel activity in rat ventricular cardiomyocytes.
Abstract Excessive increase of cytosolic Ca2+ through the activation of L-type Ca2+ channels (LTCCs) via β adrenergic receptor induces apoptosis of cardiomyocytes. Canstatin, a cleaved fragment of collagen type IV α2 chain, is abundantly expressed in normal heart tissue. We previously reported that canstatin inhibits β adrenergic receptor-stimulated apoptosis in cardiomyoblasts. Here, we tested the hyposeis that canstatin regulates LTCCs activity in ventricular cardiomyocytes. Collagen type IV α2 chain (COL4A2) small interfering (si) RNA (for canstatin suppression) or control siRNA was injected via jugular vei...
Source: Biochemical and Biophysical Research communications - April 4, 2018 Category: Biochemistry Authors: Imoto K, Hirakawa M, Okada M, Yamawaki H Tags: Biochem Biophys Res Commun Source Type: research

Patients with Long QT Syndrome Due to Impaired hERG-encoded Kv11.1 Potassium Channel Have Exaggerated Endocrine Pancreatic and Incretin Function Associated with Reactive Hypoglycemia.
Conclusions -Besides a prolonged cardiac repolarization phase, LQT2 patients display increased GLP-1, GIP and insulin secretion and defective glucagon secretion causing decreased plasma glucose and thus increased risk of hypoglycemia. Furthermore, glucose ingestion increased QT interval and aggravated the cardiac repolarization disturbances in LQT2 patients. Clinical Trial Registration -ClinicalTrials.gov Identifier: NCT02775513. PMID: 28235848 [PubMed - as supplied by publisher]
Source: Circulation - February 23, 2017 Category: Cardiology Authors: Hyltén-Cavallius L, Iepsen EW, Wewer Albrechtsen NJ, Svendstrup M, Lubberding AF, Hartmann B, Jespersen T, Linneberg A, Christiansen M, Vestergaard H, Pedersen O, Holst JJ, Kanters JK, Hansen T, Torekov SS Tags: Circulation Source Type: research

Knockdown of cardiac Kir3.1 gene with siRNA can improve bradycardia in an experimental sinus bradycardia rat model.
The objective of this study was to explore whether the inhibition of potassium inwardly rectifying channel (Kir3.1) with short interfering RNA (siRNA) can improve bradycardia in an experimental sinus bradycardia rat model. 54 Sprague Dawley (SD) rats were randomly divided into three groups: experimental group, control group, and sham group. Sinus bradycardia model was established in SD rats through chemical ablation of sinoatrial (SA) node with 20% formaldehyde. Variations of Kir3.1 expression at mRNA and protein level were examined with qPCR and Western blotting. Electrocardiograms (ECG) of rats at 3 days and 1, 2, 3, an...
Source: Molecular and Cellular Biochemistry - February 14, 2017 Category: Biochemistry Authors: Li Y, Fu X, Zhang Z, Yu B Tags: Mol Cell Biochem Source Type: research

NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy.
Authors: Treuer AV, Gonzalez DR Abstract NOS1AP gene (nitric oxide synthase 1-adaptor protein) is strongly associated with abnormalities in the QT interval of the electrocardiogram and with sudden cardiac death. To determine the role of NOS1AP in the physiology of the cardiac myocyte, we assessed the impact of silencing NOS1AP, using siRNA, on [Ca(2+)]i transients in neonatal cardiomyocytes. In addition, we examined the co-localization of NOS1AP with cardiac ion channels, and finally, evaluated the expression of NOS1AP in a mouse model of dystrophic cardiomyopathy. Using siRNA, NOS1AP levels were reduced to ~30% of...
Source: International Journal of Physiology, Pathophysiology and Pharmacology - November 16, 2014 Category: Physiology Tags: Int J Physiol Pathophysiol Pharmacol Source Type: research