Kynurenic acid (KYNA) is derived from tryptophan, formed by the kynurenic pathway. KYNA is being widely studied as a biomarker for neurological and cardiovascular diseases, as it is found in ischemic conditions as a protective agent; however, little is known about its effect after ischemia-reperfusion in the vascular system. We induced ischemia for 30 min followed by 5 min reperfusion (I/R) in the rat aorta for KYNA evaluation using functional assays combined with proteomics. KYNA recovered the exacerbated contraction induced by phenylephrine and relaxation induced by acetylcholine or sodium nitroprussiate in the I/R aorta, with vessel responses returning to values observed without I/R. The functional recovery can be related to the antioxidant activity of KYNA, which may be acting on the endothelium-injury prevention, especially during reperfusion, and to proteins that regulate neurotransmission and cell repair/growth, expressed after the KYNA treatment. These proteins interacted in a network, confirming a protein profile expression for endothelium and neuron repair after I/R. Thus, the KYNA treatment had the ability to recover the functionality of injured ischemic-reperfusion aorta, by tissue repairing and control of neurotransmitter release, which reinforces its role in the post-ischemic condition, and can be useful in the treatment of such disease.
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http://dx.doi.org/10.3390/molecules26102845 | DOI Listing |
PLoS One
January 2025
Department of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Background: The causes of reduced aerobic exercise capacity (ExCap) in chronic kidney disease (CKD) are multifactorial, possibly involving the accumulation of tryptophan (TRP) metabolites such as kynurenine (KYN) and kynurenic acid (KYNA), known as kynurenines. Their relationship to ExCap has yet to be studied in CKD. We hypothesised that aerobic ExCap would be negatively associated with plasma levels of TRP, KYN and KYNA in CKD.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
January 2025
Molecular and Cellular Exercise Physiology, Department of physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Kynurenic acid (KYNA) and quinolinic acid (QUIN) are metabolites of the kynurenine pathway of tryptophan degradation with opposing biological activities in the central nervous system. In the periphery, KYNA is known to positively affect metabolic health, whereas the effects of QUIN remain less explored. Interestingly, metabolic stressors, including exercise and obesity, differentially change the balance between circulating KYNA and QUIN.
View Article and Find Full Text PDFMolecules
December 2024
Department of Physical Pharmacy and Pharmacokinetics, Poznan University of Medical Sciences, 3 Rokietnicka Street, 60-806 Poznań, Poland.
Tryptophan (TRP) is an essential amino acid crucial for the production of many bioactive compounds. Disturbances in TRP metabolism have been revealed in various diseases, many of which are closely related to the immune system. In recent years, we have focused on finding blood-based biomarkers of successful immunotherapy in cancer.
View Article and Find Full Text PDFCells
January 2025
Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates.
The Kynurenine pathway is crucial in metabolizing dietary tryptophan into bioactive compounds known as kynurenines, which have been linked to glucose homeostasis. The aryl hydrocarbon receptor (AhR) has recently emerged as the endogenous receptor for the kynurenine metabolite, kynurenic acid (KYNA). However, the specific role of AhR in pancreatic β-cells remains largely unexplored.
View Article and Find Full Text PDFBMC Endocr Disord
January 2025
School of Public Health, Anhui Medical University, No. 81 Meishan Road, Hefei, Anhui, 230032, China.
Background: As the prevalence of metabolic syndrome (MetS) rises among older adults, the associated risks of cardiovascular diseases and diabetes significantly increase, and it is closely linked to various metabolic processes in the body. Dysregulation of tryptophan (TRP) metabolism, particularly alterations in the kynurenine (KYN) and serotonin pathways, has been linked to the onset of chronic inflammation, oxidative stress, and insulin resistance, key contributors to the development of MetS. We aim to investigate the relationship between the TRP metabolites and the risk of MetS in older adults.
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