Therapeutic Potential of Emerging NAD+-Increasing Strategies for Cardiovascular Diseases

Rotllan, Noemí; Camacho, Mercedes; Tondo, Mireia; Diarte-Añazco, Elena M G; Canyelles, Marina; Méndez-Lara, Karen Alejandra; Benı́tez, Sònia; Alonso, Núria; Escolà‐Gil, Joan Carles; Blanco‐Vaca, Francisco; Julve, Josep

doi:10.3390/antiox10121939

Cited by 13 publications

(8 citation statements)

References 271 publications

(345 reference statements)

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“…Among them, NADH is the largest protein complex in oxidative phosphorylation, and homozygous mutation in the intron of its gene will reduce the activity of the complex, thus exhibiting the clinical characteristics of hypertrophic cardiomyopathy. At the same time, Rotllan et al [ 17 ] also pointed out that in the process of ischemia-reperfusion, if the proteolysis of NDUFS7 is increased, the activity of the complex will be reduced to varying degrees, leading to the aggravation of myocardial injury, while NDUFA13 gene knockout has a protective effect on myocardium.…”

Section: Discussionmentioning

confidence: 99%

Deep Learning-Based Medical Data Association Rules to Explore the Connectivity and Regulation Mechanism of miRNA-mRNA Network in Myocarditis

Hao

et al. 2022

Computational and Mathematical Methods in Medicine

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Acute, chronic myocarditis as myocardial localized or diffuse inflammation lesions is usually involving cardiac function in patients with severe adverse outcomes such as heart failure, sudden death, and no unified, but its pathogenesis clinical is mainly composed of a number of factors including infection and autoimmune defects, such as physical and chemical factors; therefore, it is of great significance to explore the regulation mechanism of myocarditis-related miRNA network connectivity and temperament for in-depth understanding of the pathogenesis of myocarditis and the direction of targeted therapy. Based on this, this study explored the miRNA network related to the pathogenesis of myocarditis through deep learning medical data association rules and analyzed its specific mechanism. The results showed that 39 upregulated miRNAs, 88 downregulated miRNAs, 109 upregulated differentially expressed miRNAs, and 589 downregulated mRNAs were obtained by data association through GSE126677 and GSE4172 databases. GO enrichment and KRGG enrichment analysis showed that the differentially expressed mRNAs were involved in the regulation of a variety of biological processes, cellular components, and molecular functions. At the same time, the miRNA with differentially expressed miRNAs and their corresponding mRNAs were connected to further clarify the specific molecular mechanism of the pathological changes of myocarditis by constructing miRNA-mRNA network. It provides effective potential molecular targets for subsequent treatment and diagnosis.

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Section: Discussionmentioning

confidence: 99%

Deep Learning-Based Medical Data Association Rules to Explore the Connectivity and Regulation Mechanism of miRNA-mRNA Network in Myocarditis

Hao

et al. 2022

Computational and Mathematical Methods in Medicine

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“…In regard to obesity, increased body weight leads to impaired glucose tolerance that results in DM progression [14][15][16][17][18][19][20][21][22][23][24]. Obesity can especially increase the risk of developing DM in young individuals and can affect stem cell proliferation, aging, inflammation, oxidative stress injury, and mitochondrial function [25][26][27][28][29][30][31][32][33][34].…”

Section: Cellular Metabolism Dysfunctionmentioning

confidence: 99%

Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System

Maiese

2023

Biomolecules

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It is estimated that, at minimum, 500 million individuals suffer from cellular metabolic dysfunction, such as diabetes mellitus (DM), throughout the world. Even more concerning is the knowledge that metabolic disease is intimately tied to neurodegenerative disorders, affecting both the central and peripheral nervous systems as well as leading to dementia, the seventh leading cause of death. New and innovative therapeutic strategies that address cellular metabolism, apoptosis, autophagy, and pyroptosis, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), growth factor signaling with erythropoietin (EPO), and risk factors such as the apolipoprotein E (APOE-ε4) gene and coronavirus disease 2019 (COVID-19) can offer valuable insights for the clinical care and treatment of neurodegenerative disorders impacted by cellular metabolic disease. Critical insight into and modulation of these complex pathways are required since mTOR signaling pathways, such as AMPK activation, can improve memory retention in Alzheimer’s disease (AD) and DM, promote healthy aging, facilitate clearance of β-amyloid (Aß) and tau in the brain, and control inflammation, but also may lead to cognitive loss and long-COVID syndrome through mechanisms that can include oxidative stress, mitochondrial dysfunction, cytokine release, and APOE-ε4 if pathways such as autophagy and other mechanisms of programmed cell death are left unchecked.

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“…Apart from NA-mediated effects, other NAD+ precursors also exert anti-inflammatory effects by preventing inflammation in tissue-resident immune cells, such as macrophages, which are ultimately involved in the resolution of tissue inflammation [16]. Moreover, some of those precursors can also promote differentiation to macrophages with attenuated proinflammatory characteristics [16]. However, whether these effects could also be favorably influencing gastrointestinal inflammation and function has been poorly addressed.…”

Section: Introductionmentioning

confidence: 99%

NAD+ Precursors and Intestinal Inflammation: Therapeutic Insights Involving Gut Microbiota

Niño-Narvión,

Rojo-López,

Martinez-Santos

et al. 2023

Nutrients

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The oxidized form of nicotinamide adenine dinucleotide (NAD+) is a critical metabolite for living cells. NAD+ may act either as a cofactor for many cellular reactions as well as a coenzyme for different NAD+-consuming enzymes involved in the physiological homeostasis of different organs and systems. In mammals, NAD+ is synthesized from either tryptophan or other vitamin B3 intermediates that act as NAD+ precursors. Recent research suggests that NAD+ precursors play a crucial role in maintaining the integrity of the gut barrier. Indeed, its deficiency has been associated with enhanced gut inflammation and leakage, and dysbiosis. Conversely, NAD+-increasing therapies may confer protection against intestinal inflammation in experimental conditions and human patients, with accumulating evidence indicating that such favorable effects could be, at least in part, mediated by concomitant changes in the composition of intestinal microbiota. However, the mechanisms by which NAD+-based treatments affect the microbiota are still poorly understood. In this context, we have focused specifically on the impact of NAD+ deficiency on intestinal inflammation and dysbiosis in animal and human models. We have further explored the relationship between NAD+ and improved host intestinal metabolism and immunity and the composition of microbiota in vivo. Overall, this comprehensive review aims to provide a new perspective on the effect of NAD+-increasing strategies on host intestinal physiology.

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Therapeutic Potential of Emerging NAD+-Increasing Strategies for Cardiovascular Diseases

Cited by 13 publications

References 271 publications

Deep Learning-Based Medical Data Association Rules to Explore the Connectivity and Regulation Mechanism of miRNA-mRNA Network in Myocarditis

Deep Learning-Based Medical Data Association Rules to Explore the Connectivity and Regulation Mechanism of miRNA-mRNA Network in Myocarditis

Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System

NAD+ Precursors and Intestinal Inflammation: Therapeutic Insights Involving Gut Microbiota

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