The current study investigated the effect of preslaughter transport on stress response and meat quality of broilers and explored the underlying mechanisms involved in the regulation of muscle glycolysis through calcium/calmodulin-dependent protein kinase kinase (CaMKK)/AMP-activated protein kinase (AMPK) signaling. Results suggested that transport induced stress responses of broilers and caused PSE-like syndrome of pectoralis major muscle. Preslaughter transport enhanced the mRNA expressions of and , as well as the activities of glycolytic enzymes, which accelerated the breakdown of glycolytic substrates and the accumulation of lactic acid. In addition, acute stress induced abnormal intracellular calcium homeostasis by disrupting calcium channels on the cell membrane and sarcoplasmic reticulum, which led to the activation of CaMKK and promoted AMPK phosphorylation. This study provides evidence that the intracellular calcium overload and the enhancement of CaMKK/AMPK signaling are related to the accelerated muscle glycolysis of broiler chickens subjected to acute stress.
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http://dx.doi.org/10.1021/acs.jafc.2c07391 | DOI Listing |
Toxicol Appl Pharmacol
December 2024
Department of Rheumatology and Clinical Immunology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China. Electronic address:
The elevated risk of cardiovascular disease (CVD) associated with inflammatory rheumatic diseases has long been recognized. Patients with established rheumatoid arthritis (RA) have a higher mortality rate compared to the general population due to abnormal platelet activation. Thymidine phosphorylase (TYMP) plays a crucial role in platelet activation and thrombosis, following bridging the link between RA and CVD.
View Article and Find Full Text PDFBiomed Pharmacother
December 2024
Department of Biology, University of Naples Federico II, Naples, Italy; Biogem, Istituto di Biologia e Genetica Molecolare, Ariano Irpino, AV, Italy.
Intracellular Ca homeostasis dysregulation, through the modulation of calcium permeable ion channels and transporters, is gaining attention in cancer research as an apoptosis evasion mechanism. Recently, we highlighted a prognostic role for several calcium permeable channels. Among them, here, we focused on the plasma membrane bidirectional Na/Ca exchanger SLC8A1.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Mitodicure GmbH, Kriftel, Germany.
Background: Recent studies provide strong evidence for a key role of skeletal muscle pathophysiology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In a 2021 review article on the pathophysiology of ME/CFS, we postulated that hypoperfusion and ischemia can result in excessive sodium and calcium overload in skeletal muscles of ME/CFS patients to cause mitochondrial damage. Since then, experimental evidence has been provided that supports this concept.
View Article and Find Full Text PDFJ Cell Mol Med
December 2024
Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
High intake of dietary linoleic acid may increase the incidence of many diseases. The aim of this research is to examine the impact of linoleic acid on the damage caused by calcium oxalate kidney stones on renal tubular epithelial cells. Calcium oxalate monohydrate (COM) crystals were prepared and used to treat HK-2 cells, which were further treated with different concentrations of linoleic acid in vitro.
View Article and Find Full Text PDFACS Appl Mater Interfaces
December 2024
Institute of Biochemistry, Life Sciences Center, Vilnius University, Saulėtekio av. 7, Vilnius, LT-10257, Lithuania.
Neuronal cell death induced by cell membrane damage is one of the major hallmarks of neurodegenerative diseases. Neuroinflammation precedes the loss of neurons; however, whether and how inflammation-related proteins contribute to the loss of membrane integrity remains unknown. We employed a range of biophysical tools, including high-speed atomic force microscopy, fluorescence spectroscopy, and electrochemical impedance spectroscopy, to ascertain whether the pro-inflammatory protein S100A8 induces alterations in biomimetic lipid membranes upon interaction.
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