Gut microbiota and its metabolites in depression: from pathogenesis to treatment

EBioMedicine, Journal Year: 2023, Volume and Issue: 90, P. 104527 - 104527

Published: March 22, 2023

Language: Английский

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The Influence of Gut Dysbiosis in the Pathogenesis and Management of Ischemic Stroke

Cells, Journal Year: 2022, Volume and Issue: 11(7), P. 1239 - 1239

Published: April 6, 2022

Recent research on the gut microbiome has revealed influence of microbiota (GM) ischemic stroke pathogenesis and treatment outcomes. Alterations in diversity, abundance, functions microbiome, termed dysbiosis, results dysregulated gut–brain signaling, which induces intestinal barrier changes, endotoxemia, systemic inflammation, infection, affecting post-stroke Gut–brain interactions are bidirectional, signals from to brain mediated by microbially derived metabolites, such as trimethylamine N-oxide (TMAO) short-chain fatty acids (SCFAs); bacterial components, lipopolysaccharide (LPS); immune cells, T helper cells; translocation via hormonal, immune, neural pathways. Ischemic affects microbial composition hypothalamic–pituitary–adrenal (HPA) pathways, can contribute Experimental clinical studies have demonstrated that restoration usually improves outcomes regulating metabolic, inflammatory responses axis (GBA). Therefore, restoring healthy ecology may be a key therapeutic target for effective management stroke.

Language: Английский

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Mechanistic Insights into the Link between Gut Dysbiosis and Major Depression: An Extensive Review

Cells, Journal Year: 2022, Volume and Issue: 11(8), P. 1362 - 1362

Published: April 16, 2022

Depression is a highly common mental disorder, which often multifactorial with sex, genetic, environmental, and/or psychological causes. Recent advancements in biomedical research have demonstrated clear correlation between gut dysbiosis (GD) or microbial and the development of anxiety depressive behaviors. The microbiome communicates brain through neural, immune, metabolic pathways, either directly (via vagal nerves) indirectly gut- microbial-derived metabolites as well hormones endocrine peptides, including peptide YY, pancreatic polypeptide, neuropeptide Y, cholecystokinin, corticotropin-releasing factor, glucagon-like peptide, oxytocin, ghrelin). Maintaining healthy microbiota (GM) now being recognized important for health use probiotics, prebiotics, synbiotics, fecal transplantation (FMT), etc. A few approaches exert antidepressant effects via restoring GM hypothalamus–pituitary–adrenal (HPA) axis functions. In this review, we summarized etiopathogenic link depression preclinical clinical evidence. addition, collated information on recent therapies supplements, such short-chain fatty acids, vitamin B12, omega-3 etc., target gut–brain (GBA) effective management behavior anxiety.

Language: Английский

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The Role of Gut Dysbiosis in the Pathophysiology of Neuropsychiatric Disorders

Cells, Journal Year: 2022, Volume and Issue: 12(1), P. 54 - 54

Published: Dec. 23, 2022

Mounting evidence shows that the complex gut microbial ecosystem in human gastrointestinal (GI) tract regulates physiology of central nervous system (CNS) via microbiota and gut-brain (MGB) axis. The GI communicates with brain through neuroendocrine, immune, autonomic systems. Recent studies have bolstered involvement dysfunctional MGB axis signaling pathophysiology several neurodegenerative, neurodevelopmental, neuropsychiatric disorders (NPDs). Several investigations on dynamic genetic-environmental interactions (GM) shown changes composition, diversity and/or functions microbes (termed "gut dysbiosis" (GD)) affect health by inducing alterations pathways Interestingly, both preclinical clinical a positive correlation between GD pathogenesis progression NPDs. Long-term leads to overstimulation hypothalamic-pituitary-adrenal (HPA) neuroimmune system, along altered neurotransmitter levels, resulting signal transduction, inflammation, increased oxidative stress (OS), mitochondrial dysfunction, neuronal death. Further highlighted significance GM development regions specific stress-related behaviors, including depression anxiety, immune early life. GD-mediated deregulation imbalances host homeostasis significantly disrupting integrity intestinal blood-brain barrier (BBB), mucus secretion, functions. This review collates potential interaction NPDs from data. Additionally, we summarize use non-therapeutic modulators such as pro-, pre-, syn- post-biotics, diets or fecal transplantation (FMT), which are promising targets for management

Language: Английский

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Role of Endogenous Lipopolysaccharides in Neurological Disorders

Cells, Journal Year: 2022, Volume and Issue: 11(24), P. 4038 - 4038

Published: Dec. 14, 2022

Lipopolysaccharide (LPS) is a cell-wall immunostimulatory endotoxin component of Gram-negative bacteria. A growing body evidence reveals that alterations in the bacterial composition intestinal microbiota (gut dysbiosis) disrupt host immune homeostasis and barrier function. Microbial dysbiosis leads to proinflammatory milieu systemic endotoxemia, which contribute development neurodegenerative diseases metabolic disorders. Two important pathophysiological hallmarks (NDDs) are oxidative/nitrative stress inflammation, can be initiated by elevated permeability, with increased abundance pathobionts. These changes lead excessive release LPS other products into blood, turn induce chronic damages blood-brain (BBB). An impaired BBB allows translocation potentially harmful products, including LPS, activated neutrophils/leucocytes brain, results neuroinflammation apoptosis. Chronic causes neuronal damage synaptic loss, leading memory impairment. LPS-induced inflammation inappropriate activation microglia, astrocytes, dendritic cells. Consequently, these negatively affect mitochondrial function increases senescence. cellular brain give rise specific clinical symptoms, such as impairment locomotor function, muscle weakness, paralysis, learning deficits, dementia. This review summarizes contributing role cell death various diseases.

Language: Английский

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Understanding the Gut–Brain Axis and Its Therapeutic Implications for Neurodegenerative Disorders

Nutrients, Journal Year: 2023, Volume and Issue: 15(21), P. 4631 - 4631

Published: Oct. 31, 2023

The gut–brain axis (GBA) is a complex bidirectional communication network connecting the gut and brain. It involves neural, immune, endocrine pathways between gastrointestinal (GI) tract central nervous system (CNS). Perturbations of GBA have been reported in many neurodegenerative disorders (NDDs), such as Alzheimer’s disease (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS), among others, suggesting possible role pathogenesis. microbiota pivotal component GBA, alterations its composition, known dysbiosis, associated with dysfunction neurodegeneration. might influence homeostasis CNS by modulating immune and, more directly, regulating production molecules metabolites that systems, making it potential therapeutic target. Preclinical trials manipulating microbial composition through dietary intervention, probiotic prebiotic supplementation, fecal transplantation (FMT) provided promising outcomes. However, clear mechanism not well understood, results are always consistent. Here, we provide an overview major components approaches targeting to ameliorate NDDs.

Language: Английский

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Contributing roles of mitochondrial dysfunction and hepatocyte apoptosis in liver diseases through oxidative stress, post-translational modifications, inflammation, and intestinal barrier dysfunction

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: Jan. 12, 2024

Abstract This review provides an update on recent findings from basic, translational, and clinical studies the molecular mechanisms of mitochondrial dysfunction apoptosis hepatocytes in multiple liver diseases, including but not limited to alcohol-associated disease (ALD), metabolic dysfunction-associated steatotic (MASLD), drug-induced injury (DILI). While ethanol-inducible cytochrome P450-2E1 (CYP2E1) is mainly responsible for oxidizing binge alcohol via microsomal ethanol system, it also metabolizing many xenobiotics, pollutants, chemicals, drugs, specific diets abundant n-6 fatty acids, into toxic metabolites organs, liver, causing pathological insults through organelles such as mitochondria endoplasmic reticula. Oxidative imbalances (oxidative stress) promote covalent modifications lipids, proteins, nucleic acids enzymatic non-enzymatic mechanisms. Excessive changes stimulate various post-translational (PTMs) transcription factors, histones. Increased PTMs proteins inactivate enzymes involved reduction oxidative species, acid metabolism, mitophagy pathways, leading dysfunction, energy depletion, apoptosis. Unique other organelles, control signaling cascades bioenergetics (fat metabolism), inflammation, apoptosis/necrosis hepatocytes. When homeostasis shifted, these pathways become altered or shut down, likely contributing death with activation inflammation hepatic stellate cells, fibrosis cirrhosis. will encapsulate how contributes hepatocyte several types diseases order provide recommendations targeted therapeutics.

Language: Английский

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Recent advances in the epithelial barrier theory

International Immunology, Journal Year: 2024, Volume and Issue: 36(5), P. 211 - 222

Published: Jan. 16, 2024

Abstract The epithelial barrier theory links the recent rise in chronic non-communicable diseases, notably autoimmune and allergic disorders, to environmental agents disrupting barrier. Global pollution toxic agent exposure have worsened over six decades because of uncontrolled growth, modernization, industrialization, affecting human health. Introducing new chemicals without any reasonable control their health effects through these years has led documented adverse effects, especially on skin mucosal barriers. These substances, such as particulate matter, detergents, surfactants, food emulsifiers, micro- nano-plastics, diesel exhaust, cigarette smoke, ozone, been shown compromise integrity. This disruption is linked opening tight-junction barriers, inflammation, cell death, oxidative stress, metabolic regulation. Consideration must be given interplay underlying inflammatory medications, affected tissues. review article discusses detrimental effect barrier-damaging compounds involves cellular molecular mechanisms.

Language: Английский

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Complex roles of autophagy in cancer development, immune evasion, and drug resistance

Drug Resistance Updates, Journal Year: 2024, Volume and Issue: 78, P. 101170 - 101170

Published: Nov. 15, 2024

Language: Английский

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Critical Review of the Cross-Links Between Dietary Components, the Gut Microbiome, and Depression

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(2), P. 614 - 614

Published: Jan. 13, 2025

The complex relationship between diet, the gut microbiota, and mental health, particularly depression, has become a focal point of contemporary research. This critical review examines how specific dietary components, such as fiber, proteins, fats, vitamins, minerals, bioactive compounds, shape microbiome influence microbial metabolism in order to regulate depressive outcomes. These dietary-induced changes microbiota can modulate production metabolites, which play vital roles gut–brain communication. axis facilitates this communication through neural, immune, endocrine pathways. Alterations metabolites central nervous system (CNS) functions by impacting neuroplasticity, inflammatory responses, neurotransmitter levels—all are linked onset course depression. highlights recent findings linking components with beneficial composition reduced symptoms. We also explore challenges individual variability responses interventions long-term sustainability these strategies. underscores necessity for further longitudinal mechanistic studies elucidate precise mechanisms diet interactions be leveraged mitigate paving way personalized nutritional therapies.

Language: Английский

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