Metformin alleviates monoamine oxidase-related vascular oxidative stress and endothelial dysfunction in rats with diet-induced obesity

Ionică, Loredana Nicoleta; Gaiță, Laura; Bînă, Anca M.; Șoșdean, Raluca; Lighezan, Rodica; Sima, Alexandra; Malița, Daniel; Creţu, Octavian; Burlacu, Ovidiu; Muntean, Daniela-Lucia; Sturza, Adrian

doi:10.1007/s11010-021-04194-2

Cited by 15 publications

(12 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MAO-B is found in the central nervous system, where increased activity is associated with neurodegeneration and Parkinson's disease, and also found in platelets. Aging, diabetes and obesity have been associated with higher levels of monoamine oxidases [53][54][55], and they have been implicated in oxidative stress and endothelial dysfunction [56][57][58]. A recent study found an association between MAO-B activity and post-operative delirium.…”

Section: Discussionmentioning

confidence: 99%

Pseudotemporal whole blood transcriptional profiling of COVID-19 patients stratified by clinical severity reveals differences in immune responses and possible role of monoamine oxidase B

Broderick

Rivero‐Calle

Gómez-Carballa

et al. 2022

Preprint

View full text Add to dashboard Cite

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with highly variable clinical outcomes. Studying the temporal dynamics of host whole blood gene expression during SARS-CoV-2 infection can elucidate the biological processes that underlie these diverse clinical phenotypes. We employed a novel pseudotemporal approach using MaSigPro to model and compare the trajectories of whole blood transcriptomic responses in patients with mild, moderate and severe COVID-19 disease. We identified 5,267 genes significantly differentially expressed (SDE) over pseudotime and between severity groups and clustered these genes together based on pseudotemporal trends. Pathway analysis of these gene clusters revealed upregulation of multiple immune, coagulation, platelet and senescence pathways with increasing disease severity and downregulation of T cell, transcriptional and cellular metabolic pathways. The gene clusters exhibited differing pseudotemporal trends. Monoamine oxidase B was the top SDE gene, upregulated in severe>moderate>mild COVID-19 disease. This work provides new insights into the diversity of the host response to SARS-CoV-2 and disease severity and highlights the utility of pseudotemporal approaches in studying evolving immune responses to infectious diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Pseudotemporal whole blood transcriptional profiling of COVID-19 patients stratified by clinical severity reveals differences in immune responses and possible role of monoamine oxidase B

Broderick

Rivero‐Calle

Gómez-Carballa

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…1). In total, 20 references relevant to metformin and microvascular insulin resistance (32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51) were included (Tables 1 and 2).…”

Section: Methodsmentioning

confidence: 99%

Metformin's Impact on the Microvascular Response to Insulin

2022

View full text Add to dashboard Cite

Metformin improves insulin’s action on whole body glucose metabolism in various insulin-resistant populations. The detailed cellular mechanism(s) for its metabolic actions are multiple and still incompletely understood. Beyond metabolic actions, metformin also impacts microvascular function. However, the effects of metformin on microvascular function and microvascular insulin action specifically are poorly-defined. In this mini-review, we summarize what is currently known about metformin’s beneficial impact on both microvascular function and the microvascular response to insulin while highlighting methodologic issues in the literature that limit straightforward mechanistic understanding of these effects. We examine potential mechanisms for these effects based on pharmacologically-dosed studies and propose that metformin may improve human microvascular insulin resistance by attenuating oxidative stress, inflammation, and endothelial dysfunction. Finally, we explore several important evidence gaps and discuss avenues for future investigation that may clarify whether metformin’s ability to improve microvascular insulin sensitivity is linked to its positive impact on vascular outcomes.

show abstract

“…[ 305 ]. While the inhibition of complex I of ETS has been the unequivocally demonstrated as therapeutic effect and lactic acidosis as toxic one, recent work has reported the ability of metformin (applied ex vivo in a therapeutic relevant concentration, 10 microM) to decrease the expression of monoamine oxidase (MAO, an enzyme at the outer mitochondrial membrane) and the related oxidative stress in both ventricular [ 306 ] and aortic [ 307 ] murine samples.…”

Section: Mitochondrial Effects Of the Main Classes Of Drugs Used In C...mentioning

confidence: 99%

Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed

Bețiu

Noveanu

Hâncu

et al. 2022

IJMS

Self Cite

View full text Add to dashboard Cite

Mitochondria are central organelles in the homeostasis of the cardiovascular system via the integration of several physiological processes, such as ATP generation via oxidative phosphorylation, synthesis/exchange of metabolites, calcium sequestration, reactive oxygen species (ROS) production/buffering and control of cellular survival/death. Mitochondrial impairment has been widely recognized as a central pathomechanism of almost all cardiovascular diseases, rendering these organelles important therapeutic targets. Mitochondrial dysfunction has been reported to occur in the setting of drug-induced toxicity in several tissues and organs, including the heart. Members of the drug classes currently used in the therapeutics of cardiovascular pathologies have been reported to both support and undermine mitochondrial function. For the latter case, mitochondrial toxicity is the consequence of drug interference (direct or off-target effects) with mitochondrial respiration/energy conversion, DNA replication, ROS production and detoxification, cell death signaling and mitochondrial dynamics. The present narrative review aims to summarize the beneficial and deleterious mitochondrial effects of common cardiovascular medications as described in various experimental models and identify those for which evidence for both types of effects is available in the literature.

show abstract

Metformin alleviates monoamine oxidase-related vascular oxidative stress and endothelial dysfunction in rats with diet-induced obesity

Cited by 15 publications

References 55 publications

Pseudotemporal whole blood transcriptional profiling of COVID-19 patients stratified by clinical severity reveals differences in immune responses and possible role of monoamine oxidase B

Pseudotemporal whole blood transcriptional profiling of COVID-19 patients stratified by clinical severity reveals differences in immune responses and possible role of monoamine oxidase B

Metformin's Impact on the Microvascular Response to Insulin

Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed

Contact Info

Product

Resources

About