Major depression and heart failure: Interest of monoamine oxidase inhibitors

Corbineau, Sophie; Breton, Marie; Mialet‐Perez, Jeanne; Costemale-Lacoste, Jean-François

doi:10.1016/j.ijcard.2017.07.005

Cited by 30 publications

(12 citation statements)

References 54 publications

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“…Numerous nonpsychiatric inflammatory diseases, including multiple sclerosis [2], rheumatoid arthritis [3], diabetes mellitus [4], heart failure [5], and chronic kidney disease [6], are highly comorbid with MDD. A number of different lines of investigation have also provided consistent evidence for elevated C-reactive protein [7] and interleukin-6 [8] in MDD.…”

Section: Introductionmentioning

confidence: 99%

Antidepressants Improve Negative Regulation of Toll-Like Receptor Signaling in Monocytes from Patients with Major Depression

Hung¹

2018

Neuroimmunomodulation

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Objective: Changes in the brain’s inflammatory status can lead to psychopathological responses, especially depression. Using animal models, recent studies have revealed that this pathology is due, in part, to innate immune responses of monocytes. Methods: We focus on the involvement of Toll-like receptors (TLRs) and expression of genes encoding their negative regulators, SOCS1, TOLLIP, SIGIRR, MyD88s, NOD2, and TNFAIP3, in CD14⁺ monocytes from 34 patients with major depressive disorder (MDD) and 33 healthy controls before and after treatment with antidepressants. We also seek to investigate their association with depression severity, measured by the 17-item Hamilton Depression Rating Scale (HAMD-17). Results: mRNA expression of all TLRs, except TLR3 and -5, was significantly higher in monocytes from patients with MDD than in those from controls. Conversely, the “brakes” in TLR signaling, including TOLLIP, MyD88s, NOD2, and TNFAIP3, were downregulated. In clinical findings, the remission group showed higher baseline TLR4 and lower baseline IRAK3 mRNA levels but only baseline elevated SOCS1 mRNA levels, which were inversely correlated with HAMD-17 scores, predicting worsened outcome in MDD patients. In addition, TNFAIP3 mRNA levels were increased by antidepressant treatment. Conclusion: Collectively, our findings suggest a role for dysregulation of TLR signaling in monocytes in MDD and identify a balancing effect of antidepressants on this dysregulation.

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Section: Introductionmentioning

confidence: 99%

Antidepressants Improve Negative Regulation of Toll-Like Receptor Signaling in Monocytes from Patients with Major Depression

Hung¹

2018

Neuroimmunomodulation

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“…La asociación entre la FC y la depresión mayor se ha abordado desde múltiples perspectivas; desde el punto de vista siopatológico, los procesos relacionados con la disfunción cardíaca autónoma, el aumento de agentes proinamatorios y moléculas de apoptosis soluble, así como la alteración de la quimiotaxis y el incremento de la actividad neuroendocrina, entre otros, contribuyen al desarrollo de esta condición (38,39). Adicionalmente, es importante mencionar que existe un círculo vicioso entre la FC y el trastorno depresivo debido a que este último, con su impacto siológico y conductual, tiende a empeorar la FC en términos de sus resultados clínicos.…”

Section: Discussionunclassified

Validación de constructo de la escala Zung en pacientes con falla cardíaca

Rojas

Trujillo-Cáceres²,

Vargas³

et al. 2022

Investg. Enferm. Imagen Desarollo.

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Introducción: La escala Zung para depresión ha sido previamente utilizada en pacientes con falla cardíaca; sin embargo, en nuestro conocimiento no se encuentra evidencia de su validez para la versión en español y su uso en población adulta con falla cardíaca en Colombia. Objetivo: Determinar la validez de constructo de la escala Zung para depresión en su versión original y proponer una versión abreviada para pacientes adultos con falla cardíaca. Materiales y Métodos: Estudio de corte transversal, realizado en 200 pacientes de una clínica de falla y trasplante cardiaco, en quienes se aplicó Zung Self-Rating Depression Scale. Se evaluó la consistencia interna por medio del alfa de Cronbach y el análisis factorial fue utilizado para identificar las dimensiones del instrumento. Resultados: La consistencia interna de la versión original de la escala (20 ítems) fue de α=0.811. El análisis de factores mostró una estructura compuesta por tres factores que explican el 51.59% de la varianza total. La nueva versión abreviada (13 ítems) obtuvo un α=0.819 y los ítems correlacionaron con un único factor que explicó el 33.54% de la varianza total. Discusión: Nuestros hallazgos son similares a los encontrados por otros autores en diferentes poblaciones a la estudiada. Conclusiones: Se evidenció validez de constructo tanto para la escala Zung para depresión en su versión original como para la abreviada creada en la población estudiada. Sin embargo, se requieren estudios adicionales que verifiquen estos hallazgos en una muestra representativa y que otros aspectos de la psicometría sean evaluados.

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“…Elevated MAOA activity has been pointed out as a mechanism implicated in depression through producing ROS and catalyzing levels of all the three major monoamines (serotonin, norepinephrine, and dopamine) in the brain [ 57 ]. Irreversible MAO inhibitors have the potential to treat resistant depression, atypical depression, and bipolar depression, but are often reserved as back-line medicines because of their side effects [ 58 ]. Increased enzyme activity of PTGS1 and PTGS2 has been implicated as another mechanism in depression, and herb drugs reducing arachidonic acid levels through inhibiting PTGS1/2 could be used to treat depression in the chronic unpredictable mild stress rat model [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Sequencing Analysis in Obstructive Sleep Apnea and Depression: Anti-Oxidant and MAOA-Inhibiting Effects of miR-15b-5p and miR-92b-3p through Targeting PTGS1-NF-κB-SP1 Signaling

Chen

Hsu

et al. 2021

Antioxidants

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The aim of this study was to identify novel microRNAs related to obstructive sleep apnea (OSA) characterized by intermittent hypoxia with re-oxygenation (IHR) injury. Illumina MiSeq was used to identify OSA-associated microRNAs, which were validated in an independent cohort. The interaction between candidate microRNA and target genes was detected in the human THP-1, HUVEC, and SH-SY5Y cell lines. Next-generation sequencing analysis identified 22 differentially expressed miRs (12 up-regulated and 10 down-regulated) in OSA patients. Enriched predicted target pathways included senescence, adherens junction, and AGE-RAGE/TNF-α/HIF-1α signaling. In the validation cohort, miR-92b-3p and miR-15b-5p gene expressions were decreased in OSA patients, and negatively correlated with an apnea hypopnea index. PTGS1 (COX1) gene expression was increased in OSA patients, especially in those with depression. Transfection with miR-15b-5p/miR-92b-3p mimic in vitro reversed IHR-induced early apoptosis, reactive oxygen species production, MAOA hyperactivity, and up-regulations of their predicted target genes, including PTGS1, ADRB1, GABRB2, GARG1, LEP, TNFSF13B, VEGFA, and CXCL5. The luciferase assay revealed the suppressed PTGS1 expression by miR-92b-3p. Down-regulated miR-15b-5p/miR-92b-3p in OSA patients could contribute to IHR-induced oxidative stress and MAOA hyperactivity through the eicosanoid inflammatory pathway via directly targeting PTGS1-NF-κB-SP1 signaling. Over-expression of the miR-15b-5p/miR-92b-3p may be a new therapeutic strategy for OSA-related depression.

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Major depression and heart failure: Interest of monoamine oxidase inhibitors

Cited by 30 publications

References 54 publications

Antidepressants Improve Negative Regulation of Toll-Like Receptor Signaling in Monocytes from Patients with Major Depression

Antidepressants Improve Negative Regulation of Toll-Like Receptor Signaling in Monocytes from Patients with Major Depression

Validación de constructo de la escala Zung en pacientes con falla cardíaca

MicroRNA Sequencing Analysis in Obstructive Sleep Apnea and Depression: Anti-Oxidant and MAOA-Inhibiting Effects of miR-15b-5p and miR-92b-3p through Targeting PTGS1-NF-κB-SP1 Signaling

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