Cellular Signalling, Journal Year: 2025, Volume and Issue: unknown, P. 111664 - 111664
Published: Feb. 1, 2025
Language: Английский
Nature Reviews Nephrology, Journal Year: 2023, Volume and Issue: 19(5), P. 281 - 299
Published: March 23, 2023
Language: Английский
Citations
166
Biomarker Research, Journal Year: 2025, Volume and Issue: 13(1)
Published: Jan. 23, 2025
Neutrophil extracellular traps (NETs) are intricate, web-like formations composed of DNA, histones, and antimicrobial proteins, released by neutrophils. These structures participate in a wide array physiological pathological activities, including immune rheumatic diseases damage to target organs. Recently, the connection between NETs cancer has garnered significant attention. Within tumor microenvironment metabolism, exhibit multifaceted roles, such as promoting proliferation migration cells, influencing redox balance, triggering angiogenesis, driving metabolic reprogramming. This review offers comprehensive analysis link emphasizing areas that remain underexplored. include interaction with mitochondria, their effect on states within tumors, involvement reprogramming, contribution angiogenesis tumors. Such insights lay theoretical foundation for deeper understanding role development. Moreover, also delves into potential therapeutic strategies suggests future research directions, offering new perspectives treatment other related diseases.
Language: Английский
Citations
3
Nature Reviews Nephrology, Journal Year: 2025, Volume and Issue: unknown
Published: March 18, 2025
Language: Английский
Citations
2
Cell Death and Disease, Journal Year: 2023, Volume and Issue: 14(7)
Published: July 27, 2023
Abstract Pyroptosis is a novel inflammatory form of regulated cell death (RCD), characterized by swelling, membrane rupture, and pro-inflammatory effects. It recognized as potent response required for maintaining organismal homeostasis. However, excessive persistent pyroptosis contributes to severe responses accelerates the progression numerous inflammation-related disorders. In pyroptosis, activated inflammasomes cleave gasdermins (GSDMs) generate holes, releasing interleukin (IL)-1β/18, ultimately causing pyroptotic death. Mechanistically, categorized into caspase-1-mediated classical pathway caspase-4/5/11-mediated non-classical pathway. Renal fibrosis kidney disease loss structural functional units, proliferation fibroblasts myofibroblasts, extracellular matrix (ECM) accumulation, which leads interstitial tubules. Histologically, renal terminal stage chronic disease. Although there multitude newly discovered information regarding regulatory roles involved in still need be fully comprehended, how improve clinical outcomes remains obscure. Hence, this review systematically summarizes findings role pathogenesis discusses potential biomarkers drugs anti-fibrotic therapeutic strategies.
Language: Английский
Citations
32
Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 14
Published: Jan. 8, 2024
Rhodiola rosea is a valuable functional medicinal plant widely utilized in China and other Asian countries for its anti-fatigue, anti-aging, altitude sickness prevention properties. Salidroside, most active constituent derived from , exhibits potent antioxidative, hypoxia-resistant, anti-inflammatory, anticancer, anti-aging effects that have garnered significant attention. The appreciation of the pharmacological role salidroside has burgeoned over last decade, making it beneficial option treatment multiple diseases, including atherosclerosis, Alzheimer’s disease, Parkinson’s cardiovascular more. With renoprotective effects, parallel with inhibition oxidative stress inflammation, holds promise as potential therapeutic agent kidney damage. This article provides an overview microinflammatory state disease discuss current strategies, particular focus on highlighting recent advancements utilizing renal disease. mechanisms action are primarily associated regulation gene protein expression glomerular endothelial cells, podocytes, tubule mesangial cells cell carcinoma cell, TNF-α, TGF-β, IL-1β, IL-17A, IL-6, MCP-1, Bcl-2, VEGF, ECM protein, caspase-3, HIF-1α, BIM, well modulation AMPK/SIRT1, Nrf2/HO-1, Sirt1/PGC-1α, ROS/Src/Cav-1, Akt/GSK-3β, TXNIP-NLRP3, ERK1/2, TGF-β1/Smad2/3, PI3K/Akt, Wnt1/Wnt3a β-catenin, TLR4/NF-κB, MAPK, JAK2/STAT3, SIRT1/Nrf2 pathways. To best our knowledge, this review first to comprehensively cover protective diverse suggests great be developed drug metabolic syndrome, cerebrovascular diseases complications.
Language: Английский
Citations
14
Nephrology Dialysis Transplantation, Journal Year: 2024, Volume and Issue: 39(8), P. 1344 - 1359
Published: Jan. 19, 2024
ABSTRACT Background and hypothesis Acute kidney injury (AKI) could progress to chronic disease (CKD) the AKI-CKD transition has major clinical significance. A growing body of evidence unveiled role pyroptosis in injury. We postulate that GSDMD GSDME exert cumulative effects on by modulating different cellular responses. Methods established an model induced folic acid wildtype (WT), Gsdmd−/−, Gsdme−/−, Gsdmd−/−Gsdme−/− mice. Tubular injury, renal fibrosis inflammatory responses were evaluated. In vitro studies conducted investigate interplay among tubular cells, neutrophils, macrophages. Results Double deletion Gsdmd Gsdme conferred heightened protection against AKI, mitigating responses, including formation neutrophil extracellular traps (NETs), macrophage polarization differentiation, ultimately fibrosis, compared with mice single either or Gsdme. Gsdme, but not deficiency, shielded cells from pyroptosis. GSDME-dependent cell death stimulated NETs prompted towards a pro-inflammatory phenotype. deficiency suppressed subsequently hindered NETs-induced macrophage-to-myofibroblast (MMT). Conclusion collaborate contribute AKI subsequent acid. Synchronous inhibition be innovative therapeutic strategy for transition.
Language: Английский
Citations
12
Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)
Published: March 4, 2024
Abstract Hyperuricemia is an independent risk factor for chronic kidney disease (CKD) and promotes renal fibrosis, but the underlying mechanism remains largely unknown. Unresolved inflammation strongly associated with fibrosis a well-known significant contributor to progression of CKD, including hyperuricemia nephropathy. In current study, we elucidated impact Caspase-11/Gasdermin D (GSDMD)-dependent neutrophil extracellular traps (NETs) on progressive hyperuricemic We found that Caspase-11/GSDMD signaling were markedly activated in kidneys Deletion Gsdmd or Caspase-11 protects against nephropathy by reducing inflammation, proinflammatory profibrogenic factors expression, NETs generation, α-smooth muscle actin fibrosis. Furthermore, specific deletion hematopoietic cells showed protective effect Additionally, vitro studies unveiled capability uric acid inducing Caspase-11/GSDMD-dependent formation, consequently enhancing production macrophages. summary, this study demonstrated contributory role promoting which may shed new light therapeutic approach treating reversing
Language: Английский
Citations
10
Laboratory Investigation, Journal Year: 2024, Volume and Issue: 104(4), P. 100337 - 100337
Published: Jan. 22, 2024
Language: Английский
Citations
9
Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 27, 2025
Abstract Behçet's uveitis (BU) is a severe ocular manifestation of disease, typically accompanied by abnormal neutrophil infiltration and hyperactivation. However, the underlying causes excessive extracellular traps (NETs) production mechanisms which NETs contribute to pathogenesis BU remain incompletely understood. Neutrophils from patients exhibit higher propensity for release compared healthy controls. In experimental autoimmune (EAU), neutrophils are observed exert pro‐inflammatory effects through NETs. Clearing can inhibit T helper 17 (Th17) cell differentiation significantly alleviate EAU symptoms. vivo in vitro experiments demonstrate neutralizing IL‐17A markedly reducing formation EAU. Single‐cell RNA sequencing confirms that CD44 plays key role mediating interactions between Th17 cells. Antagonizing inhibits proportion cells formation. Multiplex immunofluorescence communication analyses further colocalization high CD4 + induce via upregulating CD44, turn, secrete recruit promote Interrupting NETs‐CD44‐IL‐17A feedback loop may be potential therapeutic target BU.
Language: Английский
Citations
1
Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14
Published: Sept. 27, 2023
Post-acute COVID-19 sequelae, commonly known as long COVID, encompasses a range of systemic symptoms experienced by significant number survivors. The underlying pathophysiology COVID has become topic intense research discussion. While chronic inflammation in received considerable attention, the role neutrophils, which are most abundant all immune cells and primary responders to inflammation, been unfortunately overlooked, perhaps due their short lifespan. In this review, we discuss emerging neutrophil extracellular traps (NETs) persistent inflammatory response observed patients. We present early evidence linking persistence NETs pulmonary fibrosis, cardiovascular abnormalities, neurological dysfunction COVID. Several uncertainties require investigation future studies. These include mechanisms SARS-CoV-2 brings about sustained activation phenotypes after infection resolution; whether heterogeneity neutrophils seen acute persists into phase; presence autoantibodies can induce protect them from degradation; exert differential, organ-specific effects; specifically NET components contribute pathologies, such fibrosis; senescent drive formation through pro-inflammatory secretome Answering these questions may pave way for development clinically applicable strategies targeting NETs, providing relief health crisis.
Language: Английский
Citations
23