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http://dx.doi.org/10.1016/j.chest.2018.09.032 | DOI Listing |
Arch Physiol Biochem
December 2024
Laboratory of Cardiovascular Physiology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brasil.
Animal Model Exp Med
December 2024
Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates.
Cardiac injury initiates repair mechanisms and results in cardiac remodeling and fibrosis, which appears to be a leading cause of cardiovascular diseases. Cardiac fibrosis is characterized by the accumulation of extracellular matrix proteins, mainly collagen in the cardiac interstitium. Many experimental studies have demonstrated that fibrotic injury in the heart is reversible; therefore, it is vital to understand different molecular mechanisms that are involved in the initiation, progression, and resolution of cardiac fibrosis to enable the development of antifibrotic agents.
View Article and Find Full Text PDFBMJ Case Rep
December 2024
Department of Cardiac Thoracic and Vascular Anesthesia, JSS Medical college and Hospital, Mysore, Karnataka, India.
Adverse drug reactions (ADRs) are common in clinical practice, especially among patients with multiple comorbidities and polypharmacy. The ADRs associated with medications may be minor or life-threatening. Many available ADR assessment scales and pharmacovigilance programmes have streamlined the early diagnosis and management of ADRs.
View Article and Find Full Text PDFJ Cardiovasc Pharmacol
December 2024
Laboratory of Cardiovascular Physiology, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, RS, Brasil.
Adrenergic overstimulation is detrimental to the left ventricle. However, its effects on the right ventricle (RV) are not clear. Since adrenergic overload increases metabolic demand and oxidative stress, boldine could be a therapeutic option in the treatment of cardiovascular disease due to its antioxidant role.
View Article and Find Full Text PDFBiophys Rep
October 2024
Cyrus Tang Medical Institute, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, Suzhou, Jiangsu 215123, China.
β-adrenergic receptors (βARs) play significant roles in regulating Ca signaling in cardiac myocytes, thus holding a key function in modulating heart performance. βARs regulate the influx of extracellular Ca and the release and uptake of Ca from the sarcoplasmic reticulum (SR) by activating key components such as L-type calcium channels (LTCCs), ryanodine receptors (RyRs) and phospholamban (PLN), mediated by the phosphorylation actions by protein kinase A (PKA). In cardiac myocytes, the presence of βAR provides a protective mechanism against potential overstimulation of βAR, which may aid in the restoration of cardiac dysfunctions.
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