Sex Influence on Autophagy Markers and miRNAs in Basal and Angiotensin II-Treated Human Umbilical Vein Endothelial Cells

Franconi, Flavia; Capobianco, Giampiero; Diana, Giuseppe; Lodde, Valeria; De Donno, Alberto; Idda, Maria Laura; Montella, Andrea; Campesi, Ilaria

doi:10.3390/ijms241914929

Cited by 2 publications

(1 citation statement)

References 86 publications

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“…This concatenated cellular response, which is not free of variability depending on the pathology [23][24][25], shows the real scenario that allows us not only to delve deeper into the mechanistic alterations, but also to detect potential differential markers between the two, by studying each of the possible mechanisms affected according to the key proteins that characterize them, such as LC3-II, Beclin-1, and p62 in the case of macroautophagy [26,27], or IRE-1α, PERK, and eIF2α for unfolded protein response [28]. On this basis, the cellular interactome alterations detected in patients with SCH and BD in cells at the systemic level have been the focus of the present article, in which clear differences between the two disorders have been demonstrated, supporting the possibility of molecular discrimination between them.…”

Section: Introductionmentioning

confidence: 99%

Differential Cellular Interactome in Schizophrenia and Bipolar Disorder—Discriminatory Biomarker Role

Menéndez-Valle,

Cachán-Vega,

Boga

et al. 2023

Antioxidants

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Schizophrenia (SCH) and bipolar disorder (BD) are two of the most important psychiatric pathologies due to their high population incidence and disabling power, but they also present, mainly in their debut, high clinical similarities that make their discrimination difficult. In this work, the differential oxidative stress, present in both disorders, is shown as a concatenator of the systemic alterations—both plasma and erythrocyte, and even at the level of peripheral blood mononuclear cells (PBMC)—in which, for the first time, the different affectations that both disorders cause at the level of the cellular interactome were observed. A marked erythrocyte antioxidant imbalance only present in SCH generalizes to oxidative damage at the plasma level and shows a clear impact on cellular involvement. From the alteration of protein synthesis to the induction of death by apoptosis, including proteasomal damage, mitochondrial imbalance, and autophagic alteration, all the data show a greater cellular affectation in SCH than in BD, which could be linked to increased oxidative stress. Thus, patients with SCH in our study show increased endoplasmic reticulum (ER)stress that induces increased proteasomal activity and a multifactorial response to misfolded proteins (UPR), which, together with altered mitochondrial activity, generating free radicals and leading to insufficient energy production, is associated with defective autophagy and ultimately leads the cell to a high apoptotic predisposition. In BD, however, oxidative damage is much milder and without significant activation of survival mechanisms or inhibition of apoptosis. These clear differences identified at the molecular and cellular level between the two disorders, resulting from progressive afflictions in which oxidative stress can be both a cause and a consequence, significantly improve the understanding of both disorders to date and are essential for the development of targeted and preventive treatments.

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