Prevention of New-Onset Heart Failure in Atrial Fibrillation: The Role of Pharmacological Management DOI
Amirreza Zobdeh, D Hoyle,

P. Shastri

и другие.

American Journal of Cardiovascular Drugs, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 24, 2024

Язык: Английский

Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis DOI Creative Commons
Rikke Nørregaard, Henricus A. M. Mutsaers, Jørgen Frøkiær

и другие.

Physiological Reviews, Год журнала: 2023, Номер 103(4), С. 2847 - 2892

Опубликована: Июль 13, 2023

The kidneys play a key role in maintaining total body homeostasis. complexity of this task is reflected the unique architecture organ. Ureteral obstruction greatly affects renal physiology by altering hemodynamics, changing glomerular filtration and metabolism, inducing architectural malformations kidney parenchyma, most importantly fibrosis. Persisting pathological changes lead to chronic disease, which currently ∼10% global population one major causes death worldwide. Studies on consequences ureteral date back 1800s. Even today, experimental unilateral (UUO) remains standard model for tubulointerstitial However, has certain limitations when it comes studying tubular injury repair, as well limited potential human translation. Nevertheless, provided scientific community with wealth knowledge (patho)physiology. With introduction advanced omics techniques, classical UUO remained relevant day been instrumental understanding fibrosis at molecular, genomic, cellular levels. This review details concepts recent advances obstructive nephropathy, highlighting pathophysiological hallmarks responsible functional induced obstruction, special emphasis

Язык: Английский

Процитировано

54

Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics DOI Creative Commons
Mohammad Islamuddin, Xuebin Qin

Cell Death Discovery, Год журнала: 2024, Номер 10(1)

Опубликована: Май 13, 2024

Abstract Macrophages are exceptionally diversified cell types and perform unique features functions when exposed to different stimuli within the specific microenvironment of various kidney diseases. In instances tissue necrosis or infection, patterns associated with damage pathogens prompt development pro-inflammatory macrophages (M1). These M1 contribute exacerbating damage, inflammation, eventual fibrosis. Conversely, anti-inflammatory (M2) arise in same circumstances, contributing repair regeneration processes. Impaired causes fibrosis, hence play a protective pathogenic role. response harmful body, inflammasomes, complex assemblies multiple proteins, assume pivotal function innate immunity. The initiation inflammasomes triggers activation caspase 1, which turn facilitates maturation cytokines, death. kidneys possess complete elements NLRP3 inflammasome, including NLRP3, ASC, pro-caspase-1. When activated, it caspase-1, resulting release mature proinflammatory cytokines (IL)-1β IL-18 cleavage Gasdermin D (GSDMD). This process therefore then induces pyroptosis, leading renal death, dysfunction. NLRP3–ASC–caspase-1–IL-1β–IL-18 pathway has been identified as factor pathophysiology numerous this review, we explore current progress understanding macrophage behavior concerning injury, fibrosis kidneys. Emphasizing role activated both advancement recovery phases diseases, article delves into potential strategies modify functionality also discusses emerging approaches selectively target their signaling components kidney, aiming facilitate healing

Язык: Английский

Процитировано

19

Role of mitochondria in pathogenesis and therapy of renal fibrosis DOI
Xiaodong Zhao, Yunkuo Li, Jinyu Yu

и другие.

Metabolism, Год журнала: 2024, Номер 155, С. 155913 - 155913

Опубликована: Апрель 11, 2024

Язык: Английский

Процитировано

18

The Interplay between Immune and Metabolic Pathways in Kidney Disease DOI Creative Commons
Lili Qu, Baihai Jiao

Cells, Год журнала: 2023, Номер 12(12), С. 1584 - 1584

Опубликована: Июнь 8, 2023

Kidney disease is a significant health problem worldwide, affecting an estimated 10% of the global population. encompasses diverse group disorders that vary in their underlying pathophysiology, clinical presentation, and outcomes. These include acute kidney injury (AKI), chronic (CKD), glomerulonephritis, nephrotic syndrome, polycystic disease, diabetic many others. Despite distinct etiologies, these share common feature immune system dysregulation metabolic disturbances. The pathways are intimately connected interact to modulate pathogenesis diseases. responses diseases includes complex interplay between various cell types, including resident infiltrating cells, cytokines, chemokines, complement factors. factors can trigger perpetuate inflammation, causing renal tissue progressive fibrosis. In addition, play critical roles diseases, glucose lipid metabolism, oxidative stress, mitochondrial dysfunction, altered nutrient sensing. Dysregulation contributes progression by inducing tubular injury, apoptosis, Recent studies have provided insights into intricate revealing novel therapeutic targets for prevention treatment Potential strategies modulating through targeting key or inhibiting pro-inflammatory signaling pathways, improving function, nutrient-sensing such as mTOR, AMPK, SIRT1. This review highlights importance potential implications pathways.

Язык: Английский

Процитировано

31

The Kidney in Obesity: Current Evidence, Perspectives and Controversies DOI
Dimitris Kounatidis, Natalia G. Vallianou, Theodora Stratigou

и другие.

Current Obesity Reports, Год журнала: 2024, Номер 13(4), С. 680 - 702

Опубликована: Авг. 14, 2024

Язык: Английский

Процитировано

10

Role of Peripheral NLRP3 Inflammasome in Cognitive Impairments: Insights of Non-central Factors DOI
Min Qiao, Junjun Ni,

Hong Qing

и другие.

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 25, 2025

Язык: Английский

Процитировано

1

Oleuropein attenuates the nephrotoxic effect of sunitinib in rats: Unraveling the potential role of SIRT6/Notch-1/NLRP-3/IL-1β axis DOI
Rania A. Elrashidy, Hoda E. Mohamed, Sara M. Abdel Aal

и другие.

Archives of Biochemistry and Biophysics, Год журнала: 2024, Номер 755, С. 109986 - 109986

Опубликована: Апрель 4, 2024

Язык: Английский

Процитировано

4

Cholesterol crystals in the pathogenesis of atherosclerosis DOI
Yvonne Baumer, Jason Irei, William A. Boisvert

и другие.

Nature Reviews Cardiology, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 18, 2024

Язык: Английский

Процитировано

4

Targeting the NLRP3 inflammasome as a novel therapeutic target for osteoarthritis DOI

Varnita Karmakar,

Mayukh Chain,

Ankit Majie

и другие.

Inflammopharmacology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 13, 2025

Язык: Английский

Процитировано

0

Inflammation in glomerular diseases DOI Creative Commons
Yulong Xiong, Wei Li,

Songzhi Jin

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Март 4, 2025

The structural and functional integrity of glomerular cells is critical for maintaining normal kidney function. Glomerular diseases, which involve chronic histological damage to the kidney, are related injury such as endothelial cells, mesangial (MCs), podocytes. When faced with pathogenic conditions, these release pro-inflammatory cytokines chemokines, inflammatory factors, adhesion factors. These substances interact through specific pathways, resulting in structure function glomeruli, ultimately causing disease. Although role inflammation diseases well known, molecular pathways that result remain largely unclear. For a long time, it has been believed only immune can secrete Therefore, targeted therapies against were considered first choice treating However, emerging research indicates non-immune MCs, podocytes also play renal by releasing Similarly, should be considered. This review aims uncover inflammation, time summarized glomerulus participate secreting providing valuable references future strategies prevent treat diseases. More importantly, we emphasized cell therapy, may key direction treatment

Язык: Английский

Процитировано

0