Publications by authors named "Serena Leo"

Several insults can lead to acute kidney injury (AKI) in native kidney and transplant patients, with diabetes critically contributing as pivotal risk factor. High glucose per se can disrupt several signaling pathways within the kidney that, if not restored, can favor the instauration of mechanisms of maladaptive repair, altering kidney homeostasis and proper function. Diabetic kidneys frequently show reduced oxygenation, vascular damage and enhanced inflammatory response, features that increase the kidney vulnerability to hypoxia.

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CVD remains the major cause of mortality with graft functioning in Kidney transplant recipients (KTRs), with an estimated risk of CV events about 50-fold higher than in the general population. Many strategies have been considered to reduce the CV risk such as the use of mTOR inhibitors. We evaluate whether chronic mTOR inhibition might influence CV aging in KTRs studying the molecular mechanisms involved in this effect.

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Access to renal transplantation guarantees a substantial improvement in the clinical condition and quality of life (QoL) for end-stage renal disease (ESRD) patients. In recent years, a greater number of older patients starting renal replacement therapies (RRT) have shown the long-term impact of conservative therapies for advanced CKD and the consequences of the uremic milieu, with a frail clinical condition that impacts not only their survival but also limits their access to transplantation. This process, referred to as "inflammaging," might be reversible with a tailored approach, such as RRT accompanied by specific nutritional support.

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Bisphenol A (BPA) is a contaminant whose presence in aquatic environments is increasing. In fish embryos and larvae, it severely affects cardiac development; however, its influence on the heart function of adult fish has been scarcely analyzed. This study investigated the effects of the in vivo exposure to BPA on heart physiology, morphology, and oxidative balance in the goldfish Carassius auratus.

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Angiotensin II (AngII), the principal effector of the Renin-Angiotensin System, is a pluripotent humoral agent whose biological actions include short-term modulations and long-term adaptations. In fish, short-term cardio-tropic effects of AngII are documented, but information on the role of AngII in long-term cardiac remodelling is not fully understood. Here, we describe a direct approach to disclose long-term morpho-functional effects of AngII on the zebrafish heart.

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Glomerulonephritis (GN) continues to be one of the main causes of end-stage kidney disease (ESKD) with an incidence rating from 10.5% to 38.2%.

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The extraordinary capacity of the goldfish () to increase its cardiac performance under acute hypoxia is crucial in ensuring adequate oxygen supply to tissues and organs. However, the underlying physiological mechanisms are not yet completely elucidated. By employing an ex vivo working heart preparation, we observed that the time-dependent enhancement of contractility, distinctive of the hypoxic goldfish heart, is abolished by the Nitric Oxide Synthase (NOS) antagonist L-NMMA, the Nitric Oxide (NO) scavenger PTIO, as well as by the PI3-kinase (PI3-K) and sarco/endoplasmic reticulum Ca-ATPase 2a (SERCA2a) pumps' inhibition by Wortmannin and Thapsigargin, respectively.

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The exceptional hypoxia tolerance of the goldfish heart may be achieved through the activation of an alternative mechanism recruiting the first product of the anaerobic glycolysis (i.e. piruvate).

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The goldfish () exhibits a remarkable capacity to survive and remain active under prolonged and severe hypoxia, making it a good model for studying cardiac function when oxygen availability is a limiting factor. Under hypoxia, the goldfish heart increases its performance, representing a putative component of hypoxia tolerance; however, the underlying mechanisms have not yet been elucidated. Here, we aimed to investigate the role of β3-adrenoreceptors (ARs) in the mechanisms that modulate goldfish heart performance along with the impact of oxygen levels.

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Article Synopsis
  • Selenoprotein T (SELENOT) is a protein involved in antioxidant functions, decreasing in adult mammalian tissues but re-expressing in the heart after ischemic injury, suggesting a protective role.
  • The study investigated how SELENOT and its peptide, PSELT, affect heart function in hypoxia-tolerant goldfish, finding SELENOT expression increased under acute hypoxia.
  • PSELT enhanced heart performance under normal oxygen conditions, but not under hypoxia, while also reducing markers of nitrosative stress, indicating its potential protective role in fish hearts during low oxygen situations.
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