Vascular Failure, Journal Year: 2024, Volume and Issue: 8(1), P. 24 - 34
Published: July 11, 2024
Language: Английский
Vascular Failure, Journal Year: 2024, Volume and Issue: 8(1), P. 24 - 34
Published: July 11, 2024
Language: Английский
Biosensors and Bioelectronics, Journal Year: 2024, Volume and Issue: 255, P. 116090 - 116090
Published: Feb. 5, 2024
Language: Английский
Citations
10Applied Microbiology and Biotechnology, Journal Year: 2024, Volume and Issue: 108(1)
Published: Jan. 20, 2024
Language: Английский
Citations
8International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6498 - 6498
Published: June 12, 2024
There is a “popular” belief that fat-free diet beneficial, supported by the scientific dogma indicating high levels of fatty acids promote many pathological metabolic, cardiovascular, and neurodegenerative conditions. This pressured scientists not to recognize essential role in cellular metabolism focus on detrimental effects acids. In this work, we critically review several decades studies recent publications supporting critical mitochondrial acid homeostasis Fatty are primary fuel source cell membrane building blocks from origin life. The membranes phospholipids were evolutionarily preserved earlier bacteria human subjects. past century, discovery was superseded epidemic growth metabolic conditions cardiovascular diseases. association due their “harmful” but rather result impaired abnormal lifestyle. Mitochondrial dysfunction linked drives multiple Despite flexibility, loss oxidation cannot be fully compensated for other sources substrates, such as carbohydrates amino acids, resulting pathogenic accumulation long-chain deficiency medium-chain popular belief, only energy-demanding organs heart, skeletal muscle, kidneys also metabolically “inactive” endothelial epithelial cells. Recent indicate specific tissues support cell- tissue-specific fashion. therefore, provides basis challenge these established dogmas articulate need paradigm shift “pathogenic” oxidation. important define causative develop novel therapeutic approaches targeting metabolism.
Language: Английский
Citations
7Clinical Epigenetics, Journal Year: 2024, Volume and Issue: 16(1)
Published: Nov. 29, 2024
The gut microbiota (GM) plays a critical role in regulating human physiology, with dysbiosis linked to various diseases, including heart failure (HF). HF is complex syndrome significant global health impact, as its incidence doubles each decade of life, and prevalence peaks individuals over 80 years. A bidirectional interaction exists between GM HF, where alterations can worsen the disease's progression. "gut hypothesis HF" suggests that HF-induced changes, such reduced intestinal perfusion altered motility, negatively impact composition, leading increased permeability, release GM-derived metabolites into bloodstream, systemic inflammation. This process creates vicious cycle further deteriorates function. metabolites, trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), secondary bile (BAs), influence gene expression through epigenetic mechanisms, DNA methylation histone modifications. These changes may play crucial mediating effects dysbiotic microbial linking them cardiac contributing progression HF. particularly relevant older individuals, aging itself has been associated both cumulative alterations, intensifying interplay GM, increasing risk elderly. Despite growing body evidence, modifications, remains poorly understood. dynamic nature epigenetics shaped by factors age, diet, lifestyle, presents challenges elucidating precise mechanisms underlying this relationship. Future research should prioritize innovative approaches overcome these limitations. By identifying specific metabolite-induced modifications modulating composition function novel personalized therapeutic strategies for prevention and/or treatment be developed. Moreover, targeted focusing specifically on understanding intricate connections epigenetics, during aging.
Language: Английский
Citations
6PLoS Pathogens, Journal Year: 2024, Volume and Issue: 20(3), P. e1012012 - e1012012
Published: March 8, 2024
Small molecules (less than 1,500 Da) include major biological signals that mediate host-pathogen-microbiome communication. They also key intermediates of metabolism and critical cellular building blocks. Pathogens present with unique nutritional needs restrict pathogen colonization or promote tissue damage. In parallel, parts host are responsive to immune signaling regulated by cascades. These interactions can trigger both adaptive maladaptive metabolic changes in the host, microbiome-derived contributing disease progression. turn, targeting is an important strategy develop new treatments for infectious diseases. Trypanosoma cruzi a single-celled eukaryotic causative agent Chagas disease, neglected tropical associated cardiac intestinal dysfunction. Here, we discuss role small during T . infection its vector mammalian host. We integrate these findings build theoretical interpretation how drive extrapolate on guide drug development.
Language: Английский
Citations
4Biomedicines, Journal Year: 2025, Volume and Issue: 13(2), P. 343 - 343
Published: Feb. 3, 2025
Short-chain fatty acids (SCFAs), produced through fermentation of dietary fibers by gut bacteria, play a central role in modulating cardiovascular function and heart failure (HF) development. The progression HF is influenced intestinal barrier dysfunction microbial translocation, where SCFAs serve as key mediators the gut–heart axis. This review examines complex metabolic interactions between other microbiota metabolites HF, including their relationships with trimethylamine N-oxide (TMAO), aromatic amino (AAAs), B vitamins, bile (BAs). We analyze associations SCFA production clinical parameters such left ventricular ejection fraction (LVEF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), glomerular filtration rate (GFR). Gaining insights into networks offers new potential therapeutic targets prognostic markers for managing failure, although significance needs further exploration.
Language: Английский
Citations
0Frontiers in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 12
Published: Feb. 4, 2025
Atrial cardiomyopathy is a multifaceted heart disease characterized by structural and functional abnormalities of the atria closely associated with atrial fibrillation its complications. Its etiology involves number factors, including genetic, infectious, immunologic, metabolic factors. Recent research has highlighted critical role gut microbiota in pathogenesis cardiomyopathy, this consistent gut–heart axis having major implications for cardiac health. The aim work to bridge knowledge gap regarding interactions between particular focus on elucidating mechanisms which dysbiosis may induce remodeling dysfunction. This article provides an overview changes composition effects metabolites. We also discuss how diet exercise affect influencing microbiota, as well possible future therapeutic approaches targeting axis. A healthy can prevent disease, but ecological lead variety symptoms, induction disease. pathophysiological aspects impact structure function, strategies exploring modulation treatment cardiomyopathy. Finally, we fecal transplantation oral probiotics or prebiotics. Our study highlights importance homeostasis cardiovascular health suggests that targeted interventions pave way innovative preventive
Language: Английский
Citations
0International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 2242 - 2242
Published: March 2, 2025
The effect of the gut microbiota extends beyond their habitant place from gastrointestinal tract to distant organs, including cardiovascular system. Research interest in relationship between heart and has recently been emerging. secretes metabolites, Trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), bile (BAs), indole propionic acid (IPA), hydrogen sulfide (H2S), phenylacetylglutamine (PAGln). In this review, we explore accumulating evidence on role these secreted metabolites pathophysiology ischemic non-ischemic failure (HF) by summarizing current knowledge clinical studies experimental models. Elevated TMAO contributes HF through TGF-ß/Smad signaling-mediated myocardial hypertrophy fibrosis, impairments mitochondrial energy production, DNA methylation pattern change, intracellular calcium transport. Also, high-level can promote via inflammation, histone methylation-mediated vascular platelet hyperactivity, thrombosis, as well cholesterol accumulation activation MAPK signaling. Reduced SCFAs upregulate Egr-1 protein, T-cell infiltration, HDAC 5 6 activities, leading HF, while reactive oxygen species production hyperactivation caveolin-ACE axis result HF. An altered BAs level worsens contractility, opens permeability transition pores inducing apoptosis, enhances accumulation, eventually exacerbating IPA, inhibition nicotinamide N-methyl transferase expression increased nicotinamide, NAD+/NADH, SIRT3 levels, ameliorate HF; meanwhile, H2S suppressing Nox4 ROS stimulating PI3K/AKT pathway also protect against Furthermore, PAGln affect sarcomere shortening ability myocyte contraction. This emerging field research new avenues for therapies restoring dietary interventions, prebiotics, probiotics, or fecal transplantation such normalizing circulating levels TMAO, SCFA, BAs, H2S, PAGln.
Language: Английский
Citations
0Frontiers in Cellular and Infection Microbiology, Journal Year: 2025, Volume and Issue: 15
Published: March 13, 2025
Heart failure with preserved left ventricular ejection fraction (HFpEF) is a disease that affects multiple organs throughout the body, accounting for over 50% of heart cases. HFpEF has significant impact on individuals’ life expectancy and quality life, but exact pathogenesis remains unclear. Emerging evidence implicates low-grade systemic inflammation as crucial role in onset progression HFpEF. Gut microbiota dysregulation associated metabolites alteration, including short-chain fatty acids, trimethylamine N-oxides, amino bile acids can exacerbate chronic inflammatory responses potentially contribute to In light these findings, we propose hypothesis “gut microbiota-inflammation-HFpEF axis”, positing interplay within this axis could be factor development This review focuses gut dysregulation-induced HFpEF’s etiology. It explores potential mechanisms linking cardiac dysfunction evaluates therapeutic restoring balance mitigating severity. The objective offer novel insights strategies management
Language: Английский
Citations
0Immunology, Journal Year: 2025, Volume and Issue: unknown
Published: March 24, 2025
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality globally. Recent groundbreaking preclinical clinical research underscores the pivotal role metabolite remodelling in pathology CVD. This metabolic transformation not only directly fuels progression CVD but also profoundly influences immune response within cardiovascular system. In this review, we focused on complex interactions between alterations responses during course Furthermore, explore potential therapeutic interventions that could be developed based understanding dysregulation By targeting these immunological pathways, novel strategies for prevention treatment CVDs might to improve patient outcomes reduce global burden disease.
Language: Английский
Citations
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