Resveratrol Reverses Endothelial Colony-Forming Cell Dysfunction in Adulthood in a Rat Model of Intrauterine Growth Restriction

Guillot, Estelle; Lemay, André; Allouche, Manon; Silva, S; Coppola, Hanna; Sabatier, Florence; Dignat-George, Françoise; Sarre, Alexandre; Peyter, Anne‐Christine; Simoncini, Stéphanie; Yzydorczyk, Catherine

doi:10.3390/ijms24119747

Cited by 4 publications

(2 citation statements)

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“…As mentioned above, EPCs are critical circulating components of the endothelium and are identified as key factors in endothelial repair. In this respect, resveratrol treatment can reverse EPC dysfunction by decreasing oxidative stress and increasing proliferation and capillary-like structure formation, and, by increasing the angiogenic factors like (NO), can reverse stress-induced senescence [208].…”

Section: Role Of Resveratrol In the Vascular Biology And Senescence P...mentioning

confidence: 99%

Endothelial Senescence and Its Impact on Angiogenesis in Alzheimer’s Disease

Georgieva

Tchekalarova

Iliev

et al. 2023

IJMS

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Endothelial cells are constantly exposed to environmental stress factors that, above a certain threshold, trigger cellular senescence and apoptosis. The altered vascular function affects new vessel formation and endothelial fitness, contributing to the progression of age-related diseases. This narrative review highlights the complex interplay between senescence, oxidative stress, extracellular vesicles, and the extracellular matrix and emphasizes the crucial role of angiogenesis in aging and Alzheimer’s disease. The interaction between the vascular and nervous systems is essential for the development of a healthy brain, especially since neurons are exceptionally dependent on nutrients carried by the blood. Therefore, anomalies in the delicate balance between pro- and antiangiogenic factors and the consequences of disrupted angiogenesis, such as misalignment, vascular leakage and disturbed blood flow, are responsible for neurodegeneration. The implications of altered non-productive angiogenesis in Alzheimer’s disease due to dysregulated Delta-Notch and VEGF signaling are further explored. Additionally, potential therapeutic strategies such as exercise and caloric restriction to modulate angiogenesis and vascular aging and to mitigate the associated debilitating symptoms are discussed. Moreover, both the roles of extracellular vesicles in stress-induced senescence and as an early detection marker for Alzheimer’s disease are considered. The intricate relationship between endothelial senescence and angiogenesis provides valuable insights into the mechanisms underlying angiogenesis-related disorders and opens avenues for future research and therapeutic interventions.

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Section: Role Of Resveratrol In the Vascular Biology And Senescence P...mentioning

confidence: 99%

Endothelial Senescence and Its Impact on Angiogenesis in Alzheimer’s Disease

Georgieva

Tchekalarova

Iliev

et al. 2023

IJMS

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“…have indeed revealed that RES may inhibit the growth of leukemia, breast, and colorectal cancer cells, arresting the cell cycle in the S/G2 phase transition and altering the regulatory mechanisms of apoptosis and DNA synthesis [129]. Furthermore, it induces premature senescence via ROS-mediated DNA damage [130,131]. Concerning CCA, RES has been shown to have higher cytotoxic and pro-apoptotic effects on CCA cells [129].…”

Section: Antioxidantsmentioning

confidence: 99%

Oxidative Stress and Redox-Dependent Pathways in Cholangiocarcinoma

Caligiuri,

Becatti,

Porro

et al. 2023

Antioxidants

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Cholangiocarcinoma (CCA) is a primary liver tumor that accounts for 2% of all cancer-related deaths worldwide yearly. It can arise from cholangiocytes of biliary tracts, peribiliary glands, and possibly from progenitor cells or even hepatocytes. CCA is characterized by high chemoresistance, aggressiveness, and poor prognosis. Potentially curative surgical therapy is restricted to a small number of patients with early-stage disease (up to 35%). Accumulating evidence indicates that CCA is an oxidative stress-driven carcinoma resulting from chronic inflammation. Oxidative stress, due to enhanced reactive oxygen species (ROS) production and/or decreased antioxidants, has been recently suggested as a key factor in cholangiocyte oncogenesis through gene expression alterations and molecular damage. However, due to different experimental models and conditions, contradictory results regarding oxidative stress in cholangiocarcinoma have been reported. The role of ROS and antioxidants in cancer is controversial due to their context-dependent ability to stimulate tumorigenesis and support cancer cell proliferation or promote cell death. On these bases, the present narrative review is focused on illustrating the role of oxidative stress in cholangiocarcinoma and the main ROS-driven intracellular pathways. Heterogeneous data about antioxidant effects on cancer development are also discussed.

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