Browsing by Author "Sobrevia Luarte, Luis Alberto"

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    Biomarkers of oxidative stress in maternal plasma, umbilical cord and placenta of patients with gestational diabetes: a systematic review and meta-analysis
    (2025) Etchegaray-Armijo, Karina; Bustos-Arriagada, Edson; Navarro-Rosenblatt, Deborah; Vera Peréz-Gacitua, Claudio Mauricio; Garmendia, María Luisa; Sobrevia Luarte, Luis Alberto; López Alarcon, Camilo Ignacio; Casanello Toledo, Paola Cecilia
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    Melatonin and Inflammatory Cytokines as Modulators of the Interaction Between Gestational Diabetes Mellitus and Pregnancy-Specific Urinary Incontinence
    (2025) Honório França, Danielle Cristina; França, Eduardo Luzia; Honório-França, Adenilda Cristina; Rezende Silva, Kênia Maria; Ataídes de Queiroz, Adriele; Morais, Tassiane Cristina; Honorio França, Emanuelle Carolina; Frota de Carvalho, Carolina Neiva; Gomes Fagundes-Triches, Danny Laura; Pascon Barbosa, Angélica Mércia; Paranhos Calderon, Iracema de Mattos; Sobrevia Luarte, Luis Alberto; Cunha Rudge, Marilza Vieira
    Background: The pathogenesis of developing gestational diabetes mellitus (GDM) integrated with pregnancy-specific urinary incontinence (PSUI) may be related to immunological and hormonal factors. Inflammatory cytokines influence the function and regulation of the urinary tract, and changes in melatonin concentration are a predisposing factor for smooth muscle dysfunction and cystometric changes. Objective: This study examines the influence of melatonin, MT1 and MT2 receptors, and inflammatory cytokines in the blood and urine of pregnant women with GDM and PSUI. Methods: Two hundred sixty-nine pregnant women were approached during the diagnostic investigation of GDM and answered a specifically structured questionnaire about the involuntary loss of urine. According to these criteria, mothers were divided into four groups: continent normoglycemic (NG-C), incontinent normoglycemic (NG-I), continent GDM (GDM-C), and incontinent GDM (GDM-UI). Blood and urine samples were collected to determine the levels of melatonin, melatonin sulfate, melatonin receptors (MT1 and MT2), and inflammatory cytokines. Results: Blood level of melatonin and IL-10 was lower, but MT1, MT2, IL-1β, IL-8, and TNF-α were higher in GDM-UI compared with the NG-C group. The melatonin sulfate level was lower in the urine of the GDM-UI group compared with the NG-C group. Conclusions: Maternal hyperglycemia associated with urinary incontinence generates an inflammatory environment characterized by reduced melatonin and IL-10 and increased IL-1β, IL-8, and TNF-α in the blood of mothers with GDM with UI. This environmental condition may be involved in the pathogenesis of these pathologies.
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    Placental mitochondrial impairment and its association with maternal metabolic dysfunction
    (WILEY, 2024) Grismaldo, R. Adriana; Luevano-Martinez, Luis A.; Reyes, Monserrat; Garcia-Marquez, Grecia; Garcia-Rivas, Gerardo; Sobrevia Luarte, Luis Alberto
    The placenta plays an essential role in pregnancy, leading to proper fetal development and growth. As an organ with multiple physiological functions for both mother and fetus, it is a highly energetic and metabolically demanding tissue. Mitochondrial physiology plays a crucial role in the metabolism of this organ and thus any alteration leading to mitochondrial dysfunction has a severe outcome in the development of the fetus. Pregnancy-related pathological states with a mitochondrial dysfunction outcome include preeclampsia and gestational diabetes mellitus. In this review, we address the role of mitochondrial morphology, metabolism and physiology of the placenta during pregnancy, highlighting the roles of the cytotrophoblast and syncytiotrophoblast. We also describe the relationship between preeclampsia, gestational diabetes, gestational diabesity and pre-pregnancy maternal obesity with mitochondrial dysfunction. image, Abstract figure legend Diseases of pregnancy such as preeclampsia, gestational diabetes mellitus, pre-pregnancy maternal obesity and obesity in pregnancy result in dysfunctional mitochondria, leading to altered fetal development and growth with consequences for young and adulthood. Created with BioRender.com. image
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    Swimming exercise attenuates diabetic myopathy and is associated with histological and mitochondrial changes in pregnant rats (Rattus norvegicus)
    (2026) Catinelli, Bruna Bologna; Pascon Barbosa, Angélica Mércia; Medolago Carr, Aline; Rafael Guilen de Oliveira; Bergamo Alves, Fernanda Cristina; Mosele, Franciele; Chies, Agnaldo Bruno; Felisbino, Sérgio Luis; Sobrevia Luarte, Luis Alberto; Souza Rossignoli, Patrícia de; Vieira Cunha Rudge, Marilza
    Aim: Diabetic-induced myopathy (DiM) is reversed by swimming exercise (SE) in diabetic pregnant rats. This study aims to characterise the role of muscle stem cells (MuSCs), mitochondrial adaptations, and inflammation in this process.Methods: A mild hyperglycaemic pregnant rat model was created by administering 100 mg/kg streptozotocin to Wistar female newborns on the first day of life. In adulthood, after mating, the rats were assigned to either a sedentary or exercise group. The SE protocol involved 60 min of daily swimming, 6 days per week, from gestational day 0 to 20. On gestational day 21, blood samples, rectus abdominis muscle (RAM), and soleus muscle were collected for analysis of fiber type, MuSCs count, mitochondrial adaptations, and inflammation markers.Results: The diabetic group showed a lower number of fast and slow-twitch fibers. SE increased the number of MuSCs, the MuSCs/myonuclei ratio, mitochondrial area, and count, and restored citrate synthase activity. SE also increased the MuSCs/fiber and myonuclei/fiber ratios, as well as the mitochondria number/fiber and mitochondria area/fiber ratios, showing a positive relationship between mitochondrial count and fiber number
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    The LINC complex in blood vessels: from physiology to pathological implications in arterioles
    (John Wiley and Sons Inc, 2025) Ferreira G.; Cardozo R.; Chavarria L.; Santander A.; Sobrevia Luarte, Luis Alberto; Chang W.; Gundersen G.; Nicolson G.L.
    © 2025 The Authors. The Journal of Physiology © 2025 The Physiological Society.The LINC (linker of nucleoskeleton and cytoskeleton) complex is a critical component of the cellular architecture that bridges the nucleoskeleton and cytoskeleton and mediates mechanotransduction to and from the nucleus. Though it plays important roles in all blood vessels, it is in arterioles that this complex plays a pivotal role in maintaining endothelial cell integrity, regulating vascular tone, forming new microvessels and modulating responses to mechanical and biochemical stimuli. It is also important in vascular smooth muscle cells and fibroblasts, where it possibly plays a role in the contractile to secretory phenotypic transformation during atherosclerosis and vascular ageing, and in fibroblasts' migration and inflammatory responses in the adventitia. Physiologically, the LINC complex contributes to the stability of arteriolar structure, adaptations to changes in blood flow and injury repair mechanisms. Pathologically, dysregulation or mutations in LINC complex components can lead to compromised endothelial function, vascular remodelling and exacerbation of cardiovascular diseases such as atherosclerosis (arteriolosclerosis). This review summarizes our current understanding of the roles of the LINC complex in cells from arterioles, highlighting its most important physiological functions, exploring its implications for vascular pathology and emphasizing some of its functional characteristics in endothelial cells. By elucidating the LINC complex's role in health and disease, we aim to provide insights that could improve future therapeutic strategies targeting LINC complex-related vascular disorders. (Figure presented.).