INDICATORS OF APOPTOTIC ACTIVITY IN PATIENTS WITH COMBINED STAGE II ESSENTIAL HYPERTENSION AND STAGE II-III CHRONIC OBSTRUCTIVE PULMONARY DISEASE BASED ON COMORBIDITY CLINICAL FEATURES DOI Open Access

O.S. Tyaglaya,

O. V. Kraydashenko,

Roman Kulynych

et al.

Актуальні проблеми сучасної медицини Вісник Української медичної стоматологічної академії, Journal Year: 2024, Volume and Issue: 24(4), P. 120 - 127

Published: Dec. 26, 2024

The purpose of the study is to improve diagnosis, prognosis and treatment chronic obstructive pulmonary disease stage II-III in combination with essential hypertension II based on clinical pathogenetic role apoptosis markers. Introduction. Chronic (COPD) a progressive, condition characterized by recurrent exacerbations that are primary reason for COPD patients seek medical care, accounting hospitalizations contributing mortality rates. Frequent associated reduced quality life poorer prognoses. Each episode accelerates progression COPD, exacerbating respiratory failure complicating its management. Severe pose significant threat leading cause fatal outcomes. Essential (EH), often observed course depends severity pathology bronchial tree obstruction. In such cases, it termed pulmonogenic hypertension, occurring 18–30% cases. Conversely, may develop under pre-existing hypertensive or symptomatic arterial hypertension. interplay these conditions substantially influences their aims enhance prognosis, II–III combined investigating Materials methods. results data comprehensive examination dynamic observation 121 both sexes, aged from 30 67 years, who were examined over period 2016-2018 years underwent inpatient at Zaporizhzhya Regional Clinical Hospital. divided into 3 groups, comparable age sex: main group included 40 (moderately severe course) various cardiovascular risk (average 50.81±0.99 years); 1st comparison 48 50.7±1.53 2nd consisted 33 51.68±1.22 years). To determine reference values ​​of studied indicators, 20 healthy people as control group. Results. analysis dynamics cysteine proteases revealed statistically increase markers comorbid (EH). This elevation was advancing age, longer duration, greater EH. Regression indicated strong relationship between blood caspase-7 levels future exacerbation risks, measured SAT score. best described quadratic regression model, following parameters: R = 0.73, R² 0.53, normalized 0.51, F 39.56, p < 0.001. Conclusion. Apoptotic processes play development

Language: Английский

RNA m5C methylation modification: a potential therapeutic target for SARS-CoV-2-associated myocarditis DOI Creative Commons
Yan Xiong, Yanan Li, Weiwei Qian

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: April 23, 2024

The Corona Virus Disease (COVID-19), caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), has quickly spread worldwide and resulted in significant morbidity mortality. Although most infections are mild, some patients can also develop severe fatal myocarditis. In eukaryotic RNAs, 5-methylcytosine (m5C) is a common kind of post-transcriptional modification, which involved regulating various biological processes (such as RNA export, translation, stability maintenance). With rapid development m5C modification detection technology, studies related to viral ever-increasing. These have revealed that plays an important role stages replication, including transcription translation. According recent studies, methylation regulate SARS-CoV-2 infection modulating innate immune signaling pathways. However, specific SARS-CoV-2-induced myocarditis remains unclear. Therefore, this review aims provide insights into molecular mechanisms infection. Moreover, regulatory NSUN2 host response was highlighted. This may new directions for developing therapeutic strategies SARS-CoV-2-associated

Language: Английский

Citations

5
Dachengqi decoction dispensing granule ameliorates LPS-induced acute lung injury by inhibiting PANoptosis in vivo and in vitro DOI
Mengqi Zhang,

Luorui Shang,

Fangyuan Zhou

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 336, P. 118699 - 118699

Published: Aug. 23, 2024

Language: Английский

Citations

4
KAE ameliorates LPS-mediated acute lung injury by inhibiting PANoptosis through the intracellular DNA-cGAS-STING axis DOI Creative Commons

Yonghu Chen,

Xilin Wu, Zhe Jiang

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 7, 2025

Acute lung injury (ALI) is a severe condition characterized by inflammation, tissue damage, and persistent activation of the cyclic GMP-AMP (cGAS)-stimulator interferon genes (STING) pathway, which exacerbates production pro-inflammatory mediators promotes progression ALI. Specific inhibition this pathway has been shown to alleviate ALI symptoms. Kaempferol-3-O-α-L-(4″-E-p-coumaroyl)-rhamnoside (KAE), an active compound found in flowers Angelica acutiloba Kitagawa, exhibits anti-inflammatory antioxidant properties. This study aimed investigate molecular mechanisms through KAE regulates cGAS-STING context was induced using LPS. Lung damage anti-inflammatory/antioxidant effects were assessed H&E staining, edema index, SOD, MDA, ELISA assays. NO release mitochondrial membrane potential (MMP) measured JC-1 Griess methods. The impact on PANoptosis analyzed flow cytometry, Western blot, immunofluorescence. significantly alleviated lipopolysaccharide-induced pulmonary reducing inflammatory cell infiltration, alleviating edema, enhancing capacity, decreasing levels cytokines mouse tissues. In both vitro vivo analyses, downregulated expression key components including cGAS, STING, p-TBK1, nuclear factor-κB. also reduced assembly PANoptosome, thereby attenuating apoptosis, necroptosis, pyroptosis. Additionally, inhibited cGAS restoring MMP, cytosolic DNA. improve inhibiting DNA suppressing activation, protecting cells from PANoptosis. Our findings provide valuable insights for development application novel therapeutic strategies

Language: Английский

Citations

0
The pathogenesis and management of heatstroke and heatstroke-induced lung injury DOI Creative Commons
Jian Liu, Qin Li, Zhimin Zou

et al.

Burns & Trauma, Journal Year: 2025, Volume and Issue: 13

Published: Jan. 1, 2025

In the past two decades, record-breaking heat waves have caused an increasing number of heat-related deaths, including heatstroke, globally. Heatstroke is a life-threatening systemic condition characterized by core body temperature >40°C and subsequent development multiple organ dysfunction syndrome. Lung injury well-documented complication heatstroke usually secondary cause patient death. recent years, extensive research has been conducted to investigate underlying causes heatstroke-induced lung injury. This review aims consolidate present current understanding key pathogenic mechanisms involved in addition, factors such as cytotoxicity, inflammation, oxidative stress, endothelial cell dysfunction, other are pathogenesis heatstroke. Furthermore, we also established management strategies for However, further investigation required fully understand detailed so that potentially effective means treating preventing can be developed studied.

Language: Английский

Citations

0
Special Issue “Molecular Advances and Perspectives of Lung Disease” DOI Open Access
Jiacheng Jiang, Longshuang Huang

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(3), P. 946 - 946

Published: Jan. 23, 2025

Respiratory diseases represent a significant global public health challenge, contributing to high mortality and morbidity rates worldwide [...]

Language: Английский

Citations

0
Luteolin Mitigates Acute Lung Injury Through Immune Modulation and Antinecroptosis Effects by Targeting the BTK and FLT3 Signaling Pathways DOI
Zhixing Cao,

Huanan Rao,

Wenya Yang

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: 73(9), P. 5180 - 5193

Published: Jan. 31, 2025

Overactive immune responses and lung cell damage exacerbate acute injury (ALI). Luteolin, a flavonoid commonly found in traditional herbs, shows potential as an anti-ALI agent pharmacological clinical research, although its biological mechanism is not fully understood. This study aims to investigate whether luteolin can ameliorate ALI through immune-modulatory antinecroptosis mechanisms. We that significantly inhibits the cellular activity of FLT3-dependent monocyte line MOLM-13 BTK-dependent B-cell TMD-8. Through molecular docking HTRF detection, it was confirmed BTK FLT3 enzyme by binding their kinase domains, with IC50 values 0.78 0.35 μM, respectively. In TNF-α-induced epithelial model, reduced increased expression IL1B, IL6, CXCL8 mRNAs blocking necroptosis signal TNF-α/BTK/MLKL. Furthermore, using Balb/c mouse model intratracheal LPS infusion (5 mg/kg), observed improved function pathology, regulated infiltration, death pulmonary tissues inhibiting protein phosphorylation. conclusion, acts natural inhibitor, effectively preventing both vivo vitro immune-modulating properties.

Language: Английский

Citations

0
The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies DOI Creative Commons

Shaoshan Liu,

Guifeng Zhang, Nan Li

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 1951 - 1967

Published: Feb. 1, 2025

Abstract: Osteoarthritis (OA) is a common degenerative joint disease characterized by the progressive degradation of articular cartilage, synovial inflammation, and subchondral bone remodeling. This review explores interplay between aging, PANoptosis, inflammation in OA progression. Age-related cellular immune dysfunctions, including senescence, senescence-associated secretory phenotypes (SASPs), immunosenescence, significantly contribute to degeneration. In OA, dysregulated apoptosis, necroptosis, pyroptosis, particularly chondrocytes, exacerbate cartilage damage. Apoptosis, mediated JNK pathway, reduces chondrocyte density, while necroptosis involving RIPK-1/RIPK-3 NLRP3 inflammasome, respectively, amplify destruction. Inflammatory cytokines damage-associated molecular patterns (DAMPs) further enhance these PANoptotic pathways. Current therapeutic strategies primarily focus on anti-inflammatory agents such as non-steroidal drugs (NSAIDs) corticosteroids, with growing interest anti-senescence targeting senescence SASP. Additionally, exploring PANoptosis mechanisms offers potential for innovative treatments. Keywords: osteoarthritis,

Language: Английский

Citations

0
New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses DOI Creative Commons

Xiaobo Su,

Yunjuan Sun, Aiguo Dai

et al.

APOPTOSIS, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 20, 2025

Language: Английский

Citations

0
MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells DOI Creative Commons

Zhaohui Zeng,

Xuelian Liu,

Xiang Fei

et al.

Tobacco Induced Diseases, Journal Year: 2025, Volume and Issue: 23(March), P. 1 - 9

Published: March 18, 2025

Bronchial epithelial cell damage is an important determinant of the severity chronic obstructive pulmonary (COPD). However, exact molecular mechanisms underlying this death in COPD development are not well understood. This study investigates involvement microRNA-21 (miR-21/miRNA-21) and its mechanism. A mouse model was created by exposing mice to cigarette smoke (CS) injecting them with extract (CSE). Both wild-type miR-21 knockout (miR-21-/-) were used investigate role (miR-21) exacerbating COPD. Various assays analyses performed, including HE staining, tunel enzyme-linked immunosorbent assay (ELISA), flow cytometry, quantitative real-time polymerase chain reaction (RT-qPCR), western blotting (WB) measure outcomes such as pathological morphological changes, necroptosis, apoptosis, levels inflammatory factors. Our results revealed upregulation lung tissue mice. Additionally, resulted decreased bronchial necroptosis evidenced downregulation tumor necrosis factor receptor 1 (TNFR1), phosphoryl-mixed lineage kinase domain-like protein (p-MLKL) caspase-3. apoptosis ultimately led a reduction factors damage-associated patterns (DAMPs), factor-α (TNF-α), interleukin-1β (IL- 1β), interleukin-6 (IL-6) high mobility group B1(HMGB1) lungs, thereby ameliorating findings suggest that contributes worsening disease modulating cells, providing new theoretical basis for pathogenesis disease.

Language: Английский

Citations

0
Establishment of rat model for aspiration pneumonia and potential mechanisms DOI Creative Commons

Hanbing Hu,

Junfeng Chen,

Yiru Shao

et al.

Animal Models and Experimental Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: March 20, 2025

Abstract Background Aspiration pneumonia is a severe health concern, particularly for ICU patients with impaired airway defenses. Current animal models fail to fully replicate the condition, focusing solely on chemical lung injury from gastric acid while neglecting pathogen‐induced inflammation. This gap hinders research pathogenesis and treatment, creating an urgent need clinically relevant model. study aimed develop improved rat model of aspiration by combining hydrochloric (HCl) lipopolysaccharide (LPS) administration. Methods Specific pathogen‐free Sprague Dawley rats underwent intratracheal instillation HCl LPS. Techniques included weight measurement, tracheal intubation, pulmonary function monitoring, tissue sampling HE staining scoring, bronchoalveolar lavage fluid (BALF) sampling, protein inflammatory cytokine analysis via BCA ELISA, BALF pH determination, Evans Blue dye assessment, blood gas analysis, FITC‐dextran leakage, Western blotting, electron microscopy, survival transcriptome sequencing bioinformatics. Statistical was performed using GraphPad Prism. Results The optimal involved 1.5 μL/g.wt (pH = 1) followed 20 μg/g.wt LPS after 1 h. reproduced acute injury, including damage, microvascular dysfunction, responses, hypoxemia, ventilation, recovery observed at 72 PANoptosis confirmed, characterized increased markers. Concentration‐dependent effects damage were identified, alongside elevation dysfunction. Conclusions optimized closely mimics clinical pneumonia, providing valuable tool studying pathophysiology therapeutic strategies.

Language: Английский

Citations

0