The Role of Inflammation and Fibrosis in ILD Treatment Decisions

American Journal of Respiratory and Critical Care Medicine, Год журнала: 2024, Номер 210(4), С. 392 - 400

Опубликована: Март 14, 2024

"The Role of Inflammation and Fibrosis in ILD Treatment Decisions." American Journal Respiratory Critical Care Medicine, 0(ja), pp.

Язык: Английский

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Impact of IL-32 Gene Polymorphisms on Tuberculosis Susceptibility in a Chinese Han population

Microbial Pathogenesis, Год журнала: 2025, Номер 200, С. 107313 - 107313

Опубликована: Янв. 20, 2025

Язык: Английский

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Soluble oncostatin M receptor (sOSMR): A potential biomarker in systemic sclerosis diagnosis

Clinica Chimica Acta, Год журнала: 2025, Номер 569, С. 120177 - 120177

Опубликована: Янв. 31, 2025

Язык: Английский

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Serum pentraxin 3 in relation to clinical and nailfold capillaroscopy findings in patients with systemic sclerosis

Egyptian Rheumatology and Rehabilitation, Год журнала: 2025, Номер 52(1)

Опубликована: Март 31, 2025

Abstract Background Systemic sclerosis (SSc) is a long-standing autoimmune disease identified by vascular and fibrotic changes related to injury of endothelium. Pentraxin (PTX3) has important role in innate immune processes. Recently, it been implicated microvascular alterations various diseases. Nailfold capillaroscopy (NFC) noninvasive technique used study microvasculature. The aim this current research demonstrate the relationship between serum PTX3 clinical NFC findings patients with SSc. Results Patients’ levels were raised compared healthy controls ( P < 0.001). There was positive correlation PXT3 creatinine, pulmonary artery pressure (PAP), nailfold capillary loop diameter r = 0.926, 0.947, 0.986, 0.001, respectively). However, negatively correlated density − 0.927 SSc experiencing digital ulcers had considerably elevated than not level, modified Rodnan skin score, PAP shown be correlated. Conclusion Serum level associated high PAP, larger diameter, less patients. might an indicator involvement

Язык: Английский

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Targeted Drug Delivery System for Pulmonary Fibrosis: Design and Development of Biomaterials

BIO Integration, Год журнала: 2025, Номер 6(1)

Опубликована: Янв. 1, 2025

Pulmonary fibrosis (PF) is a progressive interstitial lung disease characterized by excessive extracellular matrix deposition and tissue scarring, leading to impaired function respiratory failure. Although current treatments, such as pirfenidone nintedanib, slow progression, they fail completely halt or reverse fibrosis. Therefore, innovative therapeutic strategies are needed. Targeted drug delivery systems (TDDSs) emerging promising solutions. Biomaterials play critical roles in these enhancing specificity, availability, efficacy, while minimizing systemic toxicity. The most notable biomaterials include nanotechnology-based systems, including liposomes polymeric nanoparticles, which facilitate penetration release fibrotic tissues. Hydrogels have three-dimensional structures providing controlled sustained at inflammation sites, therefore particularly valuable PF treatment. Furthermore, biological carriers stem cells vesicles biocompatibility anti-inflammatory effects that improve outcomes. Despite the potential of clinical translation hindered several challenges, immune clearance, stability platforms, optimization retention within diseased Interdisciplinary approaches integrating precision medicine with advancements may provide solutions opening new avenues for This review discusses developments targeted PF, emphasizing importance biomaterials, mechanisms barriers involved pulmonary delivery, future perspectives overcoming limitations. ultimate goal patient outcomes revolutionizing approach treatment through advanced technologies.

Язык: Английский

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Recent Insights into Cellular and Molecular Mechanisms of Defective Angiogenesis in Systemic Sclerosis

Biomedicines, Год журнала: 2024, Номер 12(6), С. 1331 - 1331

Опубликована: Июнь 14, 2024

In systemic sclerosis (SSc, or scleroderma), defective angiogenesis, clinically manifesting with abnormal capillary architecture and severe reduction, represents a hallmark of early-stage disease, usually preceding the onset tissue fibrosis, is caused by several cellular molecular mechanisms affecting microvascular endothelial cells different outcomes. Indeed, once damaged, can be dysfunctionally activated, thus becoming unable to undergo angiogenesis promoting perivascular inflammation. They also apoptosis, transdifferentiate into profibrotic myofibroblasts, acquire senescence-associated secretory phenotype characterized release exosomes proinflammatory mediators. this narrative review, we aimed give comprehensive overview recent studies dealing underlying SSc related cell dysfunctions, mainly endothelial-to-mesenchymal transition process. We discussed potential novel vascular treatment strategies able restore angiogenic process reduce in complex disease.

Язык: Английский

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Methylation profile of CD247 and FOXP3 genes and frequency of certain HLA-DQ haplotypes in Celiac disease

Clinics and Research in Hepatology and Gastroenterology, Год журнала: 2025, Номер unknown, С. 102562 - 102562

Опубликована: Фев. 1, 2025

Язык: Английский

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The Role of CXCL4 in Systemic Sclerosis: DAMP, Auto-Antigen and Biomarker

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2421 - 2421

Опубликована: Март 7, 2025

Systemic sclerosis (SSc) is an autoimmune disease characterized by specific autoantibodies, vasculopathy and fibrosis of the skin internal organs. In SSc, chronic activation immune system largely sustained endogenous inflammatory mediators that act as damage-associated molecular patterns (DAMPs), which activate Toll-like receptors (TLRs). Major autoantigens are nucleic acids or molecules able to bind acids. It important identify solid predictive biomarkers both activity subtype. CXCL4 has been regarded a new biomarker for early SSc in recent years, here, we discuss its modulation over course after pharmacological interventions. Moreover, provide evidence CXCL4, addition being subtypes prognostic marker severity, dual pathogenic role SSc: on one hand, complex with self-nucleic acids, acts DAMP IFN-I pro-inflammatory cytokines’ release innate cells (such dendritic cells); other target antibodies T cells, functioning autoantigen. certainly interesting molecule inflammation autoimmunity, not only it may also be considered therapy target.

Язык: Английский

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The disruptive role of LRG1 on the vasculature and perivascular microenvironment

Frontiers in Cardiovascular Medicine, Год журнала: 2024, Номер 11

Опубликована: Апрель 30, 2024

The establishment of new blood vessels, and their subsequent stabilization, is a critical process that facilitates tissue growth organ development. Once established, vessels need to diversify meet the specific needs local maintain homeostasis. These processes are tightly regulated fundamental normal vessel function. mechanisms orchestrate angiogenesis maturation have been widely studied, with signaling crosstalk between endothelium perivascular cells being identified as an essential component. In disease, however, develop abnormally, existing lose specialization function, which invariably contributes disease progression. Despite considerable research into vasculopathic in our knowledge remains incomplete. Accordingly, identification angiocrine angiopathic molecules secreted by within vascular microenvironment, effect on behaviour, major objective. Over last decade glycoprotein leucine-rich α-2 1 (LRG1), has emerged significant molecule, stimulating defective angiogenesis, destabilizing vasculature mainly, but not uniquely, altering both canonical non-canonical TGF-β highly cell context dependent manner. Whilst LRG1 does possess any overt homeostatic role development maintenance, growing evidence provides compelling case for playing pleiotropic disrupting many settings. Thus, now reported damage various disorders including cancer, diabetes, chronic kidney ocular lung drive this dysfunction defined. Moreover, therapeutic targeting proposed re-establish quiescent normalized vasculature. review, we consider current status understanding pathology, its potential target.

Язык: Английский

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Interleukin-17A is a potential therapeutic target predicted by proteomics for systemic sclerosis patients at high risk of pulmonary arterial hypertension

Scientific Reports, Год журнала: 2024, Номер 14(1)

Опубликована: Ноя. 27, 2024

Abstract We explored effective therapeutic targets for systemic sclerosis (SSc) patients with high risk pulmonary arterial hypertension (PAH) by plasma proteomics analysis. A total of fifty-seven SSc were enrolled in the study and prevalence PAH was 19.3%. On other hand, 75.4% showed ratio forced vital capacity percentage/diffusing lungs carbon monoxide percentage> 1.6 met criteria PAH. Identification elevated proteins PAH, followed upstream regulator analysis, predicted interleukin (IL)-17A as a major molecule. Furthermore, we performed vitro neutralization using MT-6194, bispecific antibody targeting both IL-17A IL-6 receptor. found that MT-6194 broadly suppressed increased expression downstream molecules including IL-17A-related cytokines/chemokines, IL-17A-driven NF $$\kappa$$ B pathway IL-6-driven JAK/STAT which shown to be proteomics. Consequently, it is revealed promising target early intervention

Язык: Английский

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