Targeting monoamine oxidase to dampen NLRP3 inflammasome activation in inflammation

Sánchez‐Rodríguez, Ricardo; Munari, Fabio; Angioni, Roberta; Venegas, Francisca C.; Agnellini, Andrielly H R; Castro-Gil, María Paulette; Castegna, Alessandra; Luisetto, Roberto; Viola, Antonella; Canton, Marcella

doi:10.1038/s41423-020-0441-8

Cited by 42 publications

(34 citation statements)

References 11 publications

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“…Cardiomyocytes from Tg MAOA mice have been previously shown to present oxidation of mitochondrial DNA and severe mitochondria dysfunction exacerbating ROS production [ 9 ] that could favor the release of oxidized mitochondrial DNA fragments contributing to NLRP3 activation in macrophages. Moreover, endogenous MAOB-dependent ROS production by bone-marrow-derived macrophages has been shown to regulate NLRP3 activation [ 30 ]. Pharmacological inhibition of MAOB reduced IL-1β secretion in response to LPS/ATP-dependent inflammasome activation whereas NF-kB-dependent TNF-α production was unaffected [ 30 ], suggesting that excessive mitochondrial ROS production by Tg MAOA cardiomyocytes could have a direct role in macrophage NLRP3 activation.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, endogenous MAOB-dependent ROS production by bone-marrow-derived macrophages has been shown to regulate NLRP3 activation [ 30 ]. Pharmacological inhibition of MAOB reduced IL-1β secretion in response to LPS/ATP-dependent inflammasome activation whereas NF-kB-dependent TNF-α production was unaffected [ 30 ], suggesting that excessive mitochondrial ROS production by Tg MAOA cardiomyocytes could have a direct role in macrophage NLRP3 activation. The implication of the NLRP3 pathway in Tg MAOA mice to trigger IL-1β production by cardiac macrophages and sustain cardiac stromal cell senescence will require further investigations.…”

Section: Discussionmentioning

confidence: 99%

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Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells

Martini

Lefèvre

Sayir

et al. 2021

IJMS

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Accumulation of senescent cells in tissues during normal or accelerated aging has been shown to be detrimental and to favor the outcomes of age-related diseases such as heart failure (HF). We have previously shown that oxidative stress dependent on monoamine oxidase A (MAOA) activity in cardiomyocytes promotes mitochondrial damage, the formation of telomere-associated foci, senescence markers, and triggers systolic cardiac dysfunction in a model of transgenic mice overexpressing MAOA in cardiomyocytes (Tg MAOA). However, the impact of cardiomyocyte oxidative stress on the cardiac microenvironment in vivo is still unclear. Our results showed that systolic cardiac dysfunction in Tg MAOA mice was strongly correlated with oxidative stress induced premature senescence of cardiac stromal cells favoring the recruitment of CCR2+ monocytes and the installation of cardiac inflammation. Understanding the interplay between oxidative stress induced premature senescence and accelerated cardiac dysfunction will help to define new molecular pathways at the crossroad between cardiac dysfunction and accelerated aging, which could contribute to the increased susceptibility of the elderly to HF.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells

Martini

Lefèvre

Sayir

et al. 2021

IJMS

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“…It has been shown that H 2 O 2 produced by the mitochondrial enzyme monoamine oxidase B (MAO–B) is crucially involved in the activation of the inflammasome [ 83 ]. This remarkable study also suggested that MAO–B could be exploited as a target for therapeutic modulation of inflammatory signaling.…”

Section: Redox Biology Of Inflammationmentioning

confidence: 99%

Imaging Biomarkers for Monitoring the Inflammatory Redox Landscape in the Brain

Fernandes

Özcelik

2021

Antioxidants

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Inflammation is one key process in driving cellular redox homeostasis toward oxidative stress, which perpetuates inflammation. In the brain, this interplay results in a vicious cycle of cell death, the loss of neurons, and leakage of the blood–brain barrier. Hence, the neuroinflammatory response fuels the development of acute and chronic inflammatory diseases. Interrogation of the interplay between inflammation, oxidative stress, and cell death in neurological tissue in vivo is very challenging. The complexity of the underlying biological process and the fragility of the brain limit our understanding of the cause and the adequate diagnostics of neuroinflammatory diseases. In recent years, advancements in the development of molecular imaging agents addressed this limitation and enabled imaging of biomarkers of neuroinflammation in the brain. Notable redox biomarkers for imaging with positron emission tomography (PET) tracers are the 18 kDa translocator protein (TSPO) and monoamine oxygenase B (MAO–B). These findings and achievements offer the opportunity for novel diagnostic applications and therapeutic strategies. This review summarizes experimental as well as established pharmaceutical and biotechnological tools for imaging the inflammatory redox landscape in the brain, and provides a glimpse into future applications.

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Section: Structure and Physiological Function Of Maomentioning

confidence: 99%

“…Its main role is to catalyze the monoamines in the cell, so that the monoamines are oxidized to produce deamination. MAO acts on primary amines and their methylated secondary and tertiary amines, as well as long-chain diamines ( Tipton, 2018 ; Sánchez-Rodríguez et al, 2020 ). The amino acid sequence of MAO A and MAO B can be up to 71.1% identical ( Figure 1 ), although each enzyme has unique substrate and inhibitor specificity, MAO A firstly oxidizes serotonin or 5-HT and noradrenaline, whereas MAO B preferentially oxidizes beta-phenylethylamine ( Grimsby et al, 1997 ).…”

Section: Introductionmentioning

confidence: 99%

Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior

Jiang

et al. 2020

Front. Cell Dev. Biol.

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Major depressive disorder (MDD) is coming to be the regarded as one of the leading causes for human disabilities. Due to its complicated pathological process, the etiology is still unclear and the treatment is still targeting at the monoamine neurotransmitters. Early life stress has been known as a major cause for MDD, but how early life stress affects adult monoaminergic activity is not clear either. Recently, DNA methylation is considered to be the key mechanism of epigenetics and might play a role in early life stress induced mental illness. DNA methylation is an enzymatic covalent modification of DNA, has been one of the main epigenetic mechanisms investigated. The metabolic enzyme for the monoamine neurotransmitters, monoamine oxidases A/B (MAO A/MAO B) are the prime candidates for the investigation into the role of DNA methylation in mental disorders. In this review, we will review recent advances about the structure and physiological function of monoamine oxidases (MAO), brief narrative other factors include stress induced changes, early life stress, perinatal depression (PD) relationship with other epigenetic changes, such as DNA methylation, microRNA (miRNA). This review will shed light on the epigenetic changes involved in MDD, which may provide potential targets for future therapeutics in depression pathogenesis.

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Targeting monoamine oxidase to dampen NLRP3 inflammasome activation in inflammation

Cited by 42 publications

References 11 publications

Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells

Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal Cells

Imaging Biomarkers for Monitoring the Inflammatory Redox Landscape in the Brain

Early Life Stress Induced DNA Methylation of Monoamine Oxidases Leads to Depressive-Like Behavior

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