Biomedicines, Journal Year: 2024, Volume and Issue: 13(1), P. 4 - 4
Published: Dec. 24, 2024
The Special Issue "Molecular Mechanisms, Diagnoses, and Treatments of Respiratory Diseases" in the journal Biomedicines compiles critical advancements understanding respiratory diseases, focusing on their molecular mechanisms, diagnostic approaches, therapeutic strategies [...].
Language: Английский
Frontiers in Bioscience-Landmark, Journal Year: 2024, Volume and Issue: 29(6), P. 223 - 223
Published: June 20, 2024
Endothelial cell dysfunction is a complex process involving various causes, early and late events, subsequent consequences. This review provides an overview of each aspect outlines therapeutic interventions targeting these stages. Causes endothelial encompass spectrum risk factors including hypertension, diabetes, smoking, obesity, inflammation, oxidative stress, genetic predispositions. Early events such as activation, inflammatory response, dysregulated vasomotor tone precede like apoptosis, microvascular rarefaction. The consequences include remodelling, neovascularization, organ dysfunction, clinical manifestations, highlighting the diverse impacts across multiple systems. While depicted linearly, progression dynamic, influenced by underlying cause affected vascular bed. Understanding dynamics crucial for tailoring interventions, ranging from lifestyle modifications to targeted therapies, address causes effects effectively. Here we provide comprehensive understanding that essential developing strategies mitigate impact this dysregulation on health cardiovascular diseases progression.
Language: Английский
Citations
5
Infectious Disease Reports, Journal Year: 2025, Volume and Issue: 17(1), P. 15 - 15
Published: Feb. 13, 2025
Background/ Objectives: Long COVID or post-acute sequelae of SARS-CoV-2 infection (PASC) are symptoms that manifest despite passing the acute phase. These manifestations encompass a wide range symptoms, most common being fatigue, shortness breath, and cognitive dysfunction. Genetic predisposition is clearly involved in susceptibility individuals to developing these persistent variation severity forms. This review summarizes role genetic factors gene polymorphisms development major pulmonary vascular disorders associated with long COVID. Methods: A comprehensive current literature was conducted examine contributions complications following infection. Studies investigating linked hypertension, thromboembolism, endothelialitis were reviewed summarized. Results: Findings show specific variants contribute increased patients. Variants endothelial dysfunction, coagulation pathways, inflammatory responses have been implicated hypertension thromboembolic events. predispositions influencing integrity immune appear influence disease progression. Conclusions: Understanding mechanisms could pave way for targeted therapeutic interventions alleviate burden on patients experiencing
Language: Английский
Citations
0
Frontiers in Genetics, Journal Year: 2025, Volume and Issue: 16
Published: Feb. 17, 2025
COVID-19 severity has been linked to immune factors, with excessive responses like cytokine storms contributing mortality. However, the genetic basis of these is not well understood. This study aimed explore connection between and blood cell traits, given their close relationship immunity. GWAS summary statistics for counts were analyzed using Linkage Disequilibrium Score Regression (LDSC) estimate correlations heritabilities. For traits significant correlations, a Multi-Trait Analysis (MTAG) was performed identify pleiotropic loci shared counts. Our MTAG analysis identified four associated severity, five hospitalized cases, one locus related general patients. Among these, two novel in high-risk population, rs55779981 located near RAVER1 rs73009538 CARM1. In patients, previously unrecognized detected, namely, rs115545251 GFI1 rs3181049 RAVER1, while rs11065822 CUX2 emerged as newly locus. We also potential target genes, including those involved inflammation signaling (CARM1), endothelial dysfunction (INTS12), antiviral response (RAVER1), which may require further investigation. offers insights into overlap suggesting directions future research clinical exploration.
Language: Английский
Citations
0
International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(7), P. 3007 - 3007
Published: March 26, 2025
Diabetes is associated with an increased risk of thromboembolism. However, the effects apixaban, a factor Xa inhibitor on diabetic nephropathy, remain unknown. Six-week-old Wistar rats received single 60 mg/kg intraperitoneal injection streptozotocin to produce model type 1 diabetes. Type and non-diabetic control were treated or without apixaban orally for 8 weeks, blood kidneys obtained biochemical, real-time reverse transcription-polymerase chain reaction (RT-PCR) morphological analyses. Although treatment did not affect glycemic lipid parameters, it significantly (p < 0.01) inhibited increases in advanced glycation end products (AGEs), receptor AGEs (RAGE) mRNA protein levels, 8-hydroxy-2'-deoxyguanosine (8-OHdG), NADPH oxidase-driven superoxide generation at 14 weeks old. Compared rats, gene expression levels monocyte chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), transforming growth factor-β (TGF-β), connective tissue (CTGF), fibronectin 14-week-old which enhanced renal kidney injury (KIM-1) Mac-3, extracellular matrix accumulation kidneys, elevated urinary excretion KIM-1, all by apixaban. Urine KIM-1 positively correlated (r = 0.690) 8-OHdG 0.793) serum 0.823). Our present findings suggest that could ameliorate streptozotocin-induced partly blocking AGE-RAGE-oxidative stress axis kidneys.
Language: Английский
Citations
0
COVID, Journal Year: 2025, Volume and Issue: 5(4), P. 48 - 48
Published: March 31, 2025
The COVID-19 pandemic has led to persistent complications beyond the respiratory system, with emerging evidence highlighting role of gut dysbiosis in long COVID. Given established gut–skin axis, alterations microbiota post-COVID-19 may contribute dermatologic conditions such as eczema, acne, and rosacea. This review explores mechanisms by which SARS-CoV-2 disrupts microbiome, leading systemic inflammation skin disease. Furthermore, it examines potential interventions, including probiotics, prebiotics, dietary modifications, microbiome-targeted therapeutic strategies for post-COVID recovery. Understanding this link open new avenues treating chronic inflammatory COVID patients.
Language: Английский
Citations
0
Viruses, Journal Year: 2025, Volume and Issue: 17(4), P. 569 - 569
Published: April 15, 2025
SARS-CoV-2 has demonstrated a remarkable capacity for immune evasion. While initial studies focused on the Wuhan variant and adaptive immunity, later emerging strains such as Omicron exhibit mutations that may alter their immune-modulatory properties. We performed comprehensive review of evasion mechanisms associated with viral proteins to focus evolutionary dynamics modulation. systematically analyzed compared impact all currently known type I interferon (IFN) responses using dual-luciferase reporter assay carrying an interferon-inducible promoter. Results revealed Nsp1, Nsp5, Nsp14, ORF6 are potent IFN inhibitors conserved across strains. Notably, we identified strain-specific differences, Nsp6 Spike exhibiting enhanced suppression in Omicron, whereas Envelope protein largely retained this function. To extend these findings, investigated selected primary human endothelial cells also observed differences response higher expressing strain variant, suggesting Omicron’s adaptational contribute damped course pandemic’s trajectory.
Language: Английский
Citations
0
Published: Jan. 1, 2025
Language: Английский
Citations
0
Aging and Disease, Journal Year: 2024, Volume and Issue: unknown, P. 0 - 0
Published: Jan. 1, 2024
Premature vascular aging and endothelial cell senescence are major risk factors for cardiovascular diseases atherothrombotic disturbances, which main complications of both acute long COVID-19. The S protein SARS-CoV2, acts as the receptor binding viral infection, is able to induce cells inflammation it has been found an isolated element in circulation human tissues reservoirs months after infection. Here, we investigated whether directly deciphered some mechanisms involved. In primary cultures umbilical vein (HUVEC), SARS-CoV-2 enhanced a concentration-dependent manner cellular content DNA damage response markers (senescence-associated-β galactosidase, γH2AX), well growth-arrest effectors (p53, p21, p16). parallel, reduced availability cytoprotective proteins, such anti-aging klotho, Nrf2 or heme oxygenase-1, caused functional harm by impairing ex vivo endothelial-dependent vasorelaxation murine microvessels. These effects were prevented pharmacological inhibition NLRP3 inflammasome with MCC950. Furthermore, supplementation either recombinant klotho angiotensin-(1-7), equally protected against pro-senescence, pro-inflammatory pro-oxidant action protein. Globally, this study proposes novel disease context COVID-19 its sequelae provides clues order prevent complications.
Language: Английский
Citations
3
Frontiers in Cellular and Infection Microbiology, Journal Year: 2024, Volume and Issue: 14
Published: Oct. 18, 2024
In this mini review, we explore the complex network of inflammatory reactions incited by SARS-CoV-2 infection, which extends its reach well beyond respiratory domain to influence various organ systems. Synthesizing existing literature, it elucidates how hyperinflammation observed in COVID-19 patients affects multiple systems leading physiological impairments that can persist over long after resolution infection. By exploring systemic manifestations cascade, from acute distress syndrome (ARDS) renal impairment and neurological sequelae, review highlights profound interplay between inflammation dysfunction. synthesizing recent research clinical observations, aims provide an overview interactions complications associated with COVID-19, underscoring need for integrated approach treatment management. Understanding these effects is crucial improving patient outcomes preparing future public health challenges.
Language: Английский
Citations
3
Japanese Journal of Infectious Diseases, Journal Year: 2024, Volume and Issue: 77(6), P. 301 - 310
Published: June 27, 2024
Persistent inflammation during chronic human immunodeficiency virus (HIV) infection may affect the immune response against severe acute respiratory syndrome-coronavirus 2 (SARS- CoV-2) infection. Plasma levels of multiple proinflammatory cytokines SARS-CoV-2 were measured in people with HIV (PWH) effective combination antiretroviral therapy. There no significant differences any between severity coronavirus disease 2019 (COVID-19) PWH, while most significantly higher HIV-uninfected individuals COVID-19, suggesting that excess release by hyperinflammatory responses do not occur COVID-19 The strong associations observed individuals, particularly IFN-α/TNF-α and other cytokines, lost PWH. steady-state plasma IP-10, ICAM-1, CD62E indicating they an enhanced inflammatory state. absence several inter-cytokine correlations was vitro lipopolysaccharide stimulus-driven cytokine production These data suggest PWH are distinct from those partially because underlying state and/or impairment innate cells.
Language: Английский
Citations
1