Використання інгібіторів дипептидилпептидази 4 д ля лікування атеросклерозу DOI Open Access
Л.К. Соколова, V.M. Pushkarev,

О.I. Kovzun

et al.

Endokrynologia, Journal Year: 2024, Volume and Issue: 29(2), P. 172 - 182

Published: June 30, 2024

Запальні процеси відіграють ключову роль в атерогенезі. Рушійними силами запалення є ендотеліальна дисфункція (ЕД), цукровий діабет, змінений метаболізм ліпопротеїнів, вільні радикали, гемодинамічний стрес зсуву, гіпертонія та інші фактори. Інгібітори DPP-4 (іDPP-4), на додаток до гіпоглікемічних властивостей (підвищення рівня інкретинів посилення експресії їх рецепторів), контролюють фактори атерогенезу шляхом регуляції ліпідів крові, кров’яного тиску, послаблення ЕД окислювального стресу (ОС), гальмування запальних процесів (блокування шляху ядерний фактор каппаB (nuclear factor kappaB, NF-κB), сигналінгу TLR4, активації nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3)-інфламмасом і секреції інтерлейкіну(IL)-1β макрофагами (МФ)), стимулювання активності ендотеліальної синтази оксиду азоту (eNOS) утворення NO, пригнічення ендотеліну-1, молекул міжклітинної адгезії-1, судинної E-селектину ендотеліальних клітинах (ЕК). ІDPP4 знижують експресію субодиниць НАДФН-оксидази Nox2 p47phox аорті, зменшуючи ОС судин, сприяють зниженню вмісту трансформації МФ у тип М2 атеросклеротичних бляшках (АБ). M2-поляризація під час опосередкованої іDPP4 блокади раннього атеросклерозу (Ас) залежить від фактора стромальних клітин 1α (stromal cell-derived 1α, SDF-1α/CXCR4, відповідальним за посилену мобілізацію кровообіг хемотаксичну активність клітин-попередників (ЕКП), які беруть участь відновленні ендотелію. гальмують прогресування Ас зниження рівнів моноцитарного хемоаттрактантного білка-1 (MCP-1) ліганд хемокіну з C-C мотивом-22 сироватці крові пацієнтів. Крім того, зменшують кількість моноцитів, пригнічують некрозу пухлини-α (tumor necrosis factor, TNF-α)-індуковану міграцію моноцитів інфільтрацію МФ. Також пінистих клітин, ймовірно, інгібування Akt/АМФ-активована протеїнкіназа (AMPK) шляхів NF-κB JNK; LOX-1 CD36 протеїнкінази C, яка бере формуванні клітин; демонструють значне міграції проліферації гладкої мускулатури, що призводить зменшення товщини інтими, захисну рестенозі; підвищують рівень циркулюючого протизапального IL-10, відсоток Т-лімфоцитів АБ.

Mechanistic insights from inflammasome structures DOI
Jianing Fu, Kate Schroder, Hao Wu

et al.

Nature reviews. Immunology, Journal Year: 2024, Volume and Issue: 24(7), P. 518 - 535

Published: Feb. 19, 2024

Language: Английский

Citations

64
Fatal attractions that trigger inflammation and drive atherosclerotic disease DOI Creative Commons
Hitesh Sharma, Karen L. Mossman, Richard C. Austin

et al.

European Journal of Clinical Investigation, Journal Year: 2024, Volume and Issue: 54(5)

Published: Jan. 29, 2024

Abstract Background Atherosclerosis is the salient, underlying cause of cardiovascular diseases, such as arrhythmia, coronary artery disease, cardiomyopathy, pulmonary embolism and myocardial infarction. In recent years, atherosclerosis pathophysiology has evolved from a lipid‐based to an inflammation‐centric ideology. Methods This narrative review comprised original articles that were found through PubMed search engine. The following terms or amalgamation used: “cardiovascular disease,” “atherosclerosis,” “inflammation,” “GRP78,” “Hsp60,” “oxidative low‐density lipoproteins,” “aldehyde dehydrogenase,” “β2‐glycoprotein,” “lipoprotein lipase A,” “human cytomegalovirus.” “SARS‐CoV‐2,” “ chlamydia pneumonia ,” “autophagy,” “thrombosis” “therapeutics.” Results Emerging evidence supports concept associated with interaction between cell surface expression stress response chaperones, including GRP78 Hsp60, their respective autoantibodies. Moreover, various other autoantigens autoantibodies have displayed compelling connection development atherosclerosis, oxidative lipoproteins, aldehyde dehydrogenase, β2‐glycoprotein lipoprotein A. progression also concurrent viral bacterial activators diseases. will focus on contributions human cytomegalovirus well SARS‐CoV‐2 in development. Notably, autoantigen presence foreign antigen can enhance inflammation development, which leads atherosclerotic lesion progression. Conclusion We highlight discuss complex role autoantibodies, antigens lesions relationship pro‐inflammatory responses.

Language: Английский

Citations

9
Shared pyroptosis pathways and crosstalk genes underpin inflammatory links between periodontitis and atherosclerosis DOI Creative Commons

Pin-Xin Zhan,

Zhiying Feng,

Xinqi Huang

et al.

Immunobiology, Journal Year: 2025, Volume and Issue: 230(2), P. 152880 - 152880

Published: Feb. 14, 2025

Language: Английский

Citations

1
Mechanisms of NLRP3 inflammasome activation and the development of peptide inhibitors DOI
Ye Tao,

Weiyan Tao,

Xiaoyi Chen

et al.

Cytokine & Growth Factor Reviews, Journal Year: 2023, Volume and Issue: 74, P. 1 - 13

Published: Oct. 1, 2023

Language: Английский

Citations

18
Diabetic Cardiomyopathy—From Basics through Diagnosis to Treatment DOI Creative Commons
Ewa Radzioch, Bartłomiej Dąbek,

Marta Balcerczyk-Lis

et al.

Biomedicines, Journal Year: 2024, Volume and Issue: 12(4), P. 765 - 765

Published: March 29, 2024

Diabetic cardiomyopathy (DCM) is the development of myocardial dysfunction in patients with diabetes despite absence comorbidities such as hypertension, atherosclerosis or valvular defect. The cardiovascular complications poorly controlled are very well illustrated by U.K. Prospective Diabetes Study (UKPDS), which showed a clear association between increasing levels glycated hemoglobin and heart failure (HF). incidence HF projected to increase significantly, why its proper diagnosis treatment so important. Providing appropriate therapy focusing on antidiabetic hypolipemic consideration pharmacotherapy for reduces risk CMD complications. Health-promoting changes made low-carbohydrate diet, regular exercise weight reduction also appear be important achieving outcomes. New hope therapies DCM offered novel methods using stem cells miRNA, which, however, require more thorough research confirm their efficacy.

Language: Английский

Citations

8
Legume-derived bioactive peptides: role in cardiovascular disease prevention and control DOI Creative Commons

David Fonseca Hernandez,

Luis Mojica, Elvira González de Mejı́a

et al.

Current Opinion in Food Science, Journal Year: 2024, Volume and Issue: 56, P. 101132 - 101132

Published: Feb. 1, 2024

Language: Английский

Citations

7
Modulation of atherosclerosis‐related signaling pathways by Chinese herbal extracts: Recent evidence and perspectives DOI
Changxing Liu, Xinyi Guo, Xulong Zhang

et al.

Phytotherapy Research, Journal Year: 2024, Volume and Issue: 38(6), P. 2892 - 2930

Published: April 5, 2024

Abstract Atherosclerotic cardiovascular disease remains a preeminent cause of morbidity and mortality globally. The onset atherosclerosis underpins the emergence ischemic diseases, including coronary heart (CHD). Its pathogenesis entails multiple factors such as inflammation, oxidative stress, apoptosis, vascular endothelial damage, foam cell formation, platelet activation. Furthermore, it triggers activation diverse signaling pathways Phosphatidylinositol 3‐kinase/protein kinase B (PI3K/Akt), NF‐E2‐related factor 2/antioxidant response element (Nrf2/ARE), Notch pathway, peroxisome proliferator‐activated receptor (PPAR), nucleotide oligo‐structural domain‐like thermoprotein structural domain‐associated protein 3 (NLRP3), silencing information regulator 2‐associated enzyme 1 (Sirt1), nuclear transcription factor‐κB (NF‐κB), Circular RNA (Circ RNA), MicroRNA (mi Transforming growth factor‐β (TGF‐β), Janus kinase‐signal transducer activator (JAK/STAT). Over recent decades, therapeutic approaches for have been dominated by utilization high‐intensity statins to reduce lipid levels, despite significant adverse effects. Consequently, there is growing interest in development safer more efficacious drugs modalities. Traditional Chinese medicine (TCM) offers vital strategy prevention treatment diseases. Numerous studies detailed mechanisms through which TCM active ingredients modulate molecules influence atherosclerotic process. This article reviews implicated advancements research on extracts treatment, drawing original articles from various databases Google Scholar, Medline, CNKI, Scopus, Pubmed. objective furnish reference clinical management

Language: Английский

Citations

7
Harnessing Pyroptosis for Lung Cancer Therapy: The Impact of NLRP3 Inflammasome Activation DOI
Rajiv Dahiya, Vijaykumar Sutariya, Sheeba Varghese Gupta

et al.

Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 260, P. 155444 - 155444

Published: Aug. 1, 2024

Language: Английский

Citations

4
Mechanisms and Therapeutic Strategies for NLRP3 Degradation via Post-Translational Modifications in Ubiquitin-proteasome and Autophagy Lysosomal Pathway DOI

Kaiyue Su,

Minghai Tang, Jie Wu

et al.

European Journal of Medicinal Chemistry, Journal Year: 2025, Volume and Issue: 289, P. 117476 - 117476

Published: March 4, 2025

Language: Английский

Citations

0
“The Ameliorative Effect of Interleukin-17A Neutralization on Doxorubicin-Induced Cardiotoxicity by Modulating the NF-κB/NLRP3/Caspase-1/IL-1β Signaling Pathway in Rats” DOI Creative Commons

Mostafa D. Hassen,

Nahla O. Mousa,

Sara M. Radwan

et al.

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

Published: March 10, 2025

Doxorubicin (DOX) is used as a chemotherapeutic drug for treating cancer. Nevertheless, it causes damage to the heart by activating inflammatory pathways, resulting in cardiotoxicity. Imbalance cytokine production crucial component that might trigger initiation of processes. Inflammatory cytokines could be targeted therapies against cardiovascular diseases (CVDs). Interleukin-17A (IL-17A) promotes inflammation and stimulates harmful immunological reactions. The objective study was determine efficacy secukinumab (SEC), completely human monoclonal IgG1/κ antibody targets IL-17A, ameliorating DOX-induced cardiotoxicity (DIC). We administered 2.5 mg/kg DOX intraperitoneally male Wistar rats three times week 2 weeks simultaneously 0.9 SEC along with injection duration two weeks. findings indicated induced tissue, significant rise indicators (P < 0.001), well oxidative stress inflammation. DIC may have arisen from DOX's activation Pyrin domain containing 3 (NLRP3) inflammasome nuclear factor kappa beta (NF-κB) pathway. co-administration successfully reversed all abnormalities restoring cardiac functions their baseline levels, decreasing levels mediators such IL-17A interleukin-1β (IL-1β), improving reducing malondialdehyde (MDA) increasing reduced glutathione (GSH). Furthermore, mitigated heightened NF-κB/NLRP3 pathway caused DOX. This shows neutralization can prevent regulating NF-κB/NLRP3/Caspase-1/IL-1β potential therapeutic target CVDs.

Language: Английский

Citations

0