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001-es BibID:	BIBFORM132124
035-os BibID:	(scopus)105007024631 (wos)001497569600001
Első szerző:	Tóth Andrea (molekuláris biológus)
Cím:	Hypoxia-Induced Changes in Endothelial Cell Phenotype and Function / Tóth Andrea, Jeney Viktória
Dátum:	2025
ISSN:	1523-0864
Megjegyzések:	Significance: Endothelial cells (ECs) are specialized cells lining the interior surface of blood vessels, playing a crucial role in vascular biology. They exhibit remarkable versatility, adapting to various tissue requirements. Their ability to respond to physiological and pathological stimuli ensures proper tissue function and homeostasis. Recent Advances: Hypoxia is when the oxygen level in a given organ, tissue, or cell type drops below the physiological level and is insufficient to maintain adequate homeostasis. ECs respond to hypoxia by activating various mechanisms. Hypoxia-induced changes in ECs can promote survival in low-oxygen environments by altering cellular metabolism and inducing neoangiogenesis. However, hypoxia-induced EC responses can also be detrimental, leading to increased production of reactive oxygen species, heightened inflammation, changes in vascular tone, increased permeability of the endothelial barrier, and a higher risk of coagulation. Critical Issues: Hypoxia-induced EC responses contribute to the pathogenesis of various diseases, including metabolic diseases (e.g., diabetes, chronic kidney disease), infectious diseases, chronic inflammation, neoplastic diseases, cardiovascular diseases (e.g., atherosclerosis, myocardial infarction, and stroke) lung diseases (e.g., chronic obstructive pulmonary disease and pulmonary hypertension), eye diseases (age-related macular degeneration and retinopathy), and neurodegenerative diseases (e.g., Alzheimer's disease and Parkinson's disease). Future Directions: Detailed, disease-specific investigations are essential to delineate how endothelial hypoxia responses contribute to various pathologies. Understanding these mechanisms could reveal whether targeting endothelial hypoxia holds therapeutic potential. Antioxid. Redox Signal. 00, 000?000.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk hypoxia endothelial cell reactive oxygen species metabolism atherosclerosis inflammation
Megjelenés:	Antioxidants & Redox Signaling. - 43 : 16-18 (2025), p. 849-868. -
További szerzők:	Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:	NKFIH K146669 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM089746
Első szerző:	Tóth Andrea (molekuláris biológus)
Cím:	Regulation of Vascular Calcification by Reactive Oxygen Species / Tóth Andrea, Balogh Enikő, Jeney Viktória
Dátum:	2020
ISSN:	2076-3921
Megjegyzések:	Vascular calcification is the deposition of hydroxyapatite crystals in the medial or intimal layers of arteries that is usually associated with other pathological conditions including but not limited to chronic kidney disease, atherosclerosis and diabetes. Calcification is an active, cell-regulated process involving the phenotype transition of vascular smooth muscle cells (VSMCs) from contractile to osteoblast/chondrocyte-like cells. Diverse triggers and signal transduction pathways have been identified behind vascular calcification. In this review, we focus on the role of reactive oxygen species (ROS) in the osteochondrogenic phenotype switch of VSMCs and subsequent calcification. Vascular calcification is associated with elevated ROS production. Excessive ROS contribute to the activation of certain osteochondrogenic signal transduction pathways, thereby accelerating osteochondrogenic transdifferentiation of VSMCs. Inhibition of ROS production and ROS scavengers and activation of endogenous protective mechanisms are promising therapeutic approaches in the prevention of osteochondrogenic transdifferentiation of VSMCs and subsequent vascular calcification. The present review discusses the formation and actions of excess ROS in different experimental models of calcification, and the potential of ROS-lowering strategies in the prevention of this deleterious condition.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk vascular calcification reactive oxygen species (ROS) vascular smooth muscle cells (VSMCs) osteochondrogenic transdifferentiation Runx2
Megjelenés:	Antioxidants. - 9 : 10 (2020), p. 1-24. -
További szerzők:	Balogh Enikő (1987-) (molekuláris biológus) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:	K131535 NKFIH
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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