Advances in Clinical Medicine, Journal Year: 2024, Volume and Issue: 14(09), P. 758 - 764
Published: Jan. 1, 2024
Language: Английский
Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 91 - 103
Published: Jan. 1, 2025
Both renal function decline and systemic inflammation may synergistically increase the risk of atrial fibrillation (AF). This study investigates association between estimated glomerular filtration rate (eGFR) high-sensitivity C-reactive protein (hs-CRP) levels with new-onset AF in patients diabetes mellitus. We included diabetic without who participated physical exams Kailuan Study from 2006 to 2010. Participants were categorized into four groups based on baseline eGFR hs-CRP levels: 1) high (≥60 mL/min/1.73m²) low (<3 mg/L) (n=6,915), 2) (≥3 (n=3,154), 3) (<60 (n=4,638), 4) (n=1,809). employed multivariable Cox regression analysis evaluate relationships eGFR, hs-CRP, AF, adjusting for confounders including smoking status, alcohol consumption, blood pressure, fasting glucose (FBG), heart rate, lipid levels, body mass index (BMI), medication usage. Competing was also performed. Among 16,516 patients, 222 developed over a mean follow-up 12.6 years. After confounders, elevated reduced significantly associated higher compared eGFR/low group. These findings remained consistent after excluding cases within first 2-year. No significant interaction observed (P=0.227). Subgroup revealed that combination had predictive value primarily males under 60 years age, individuals FBG <9 mmol/L, hypertension, those not hypoglycemic medications. In decreased independently linked an increased emphasizing importance monitoring these factors early detection prevention AF.
Language: Английский
Citations
2
Journal of the American College of Cardiology, Journal Year: 2024, Volume and Issue: 83(20), P. 2015 - 2027
Published: May 1, 2024
Language: Английский
Citations
15
European Heart Journal, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 17, 2025
Enhanced inflammatory signalling causally contributes to atrial fibrillation (AF) development. Gasdermin D (GSDMD) is an important downstream effector of several inflammasome pathways. However, the role GSDMD, particularly cleaved N-terminal (NT)-GSDMD, in non-immune cells remains elusive. This study aimed elucidate function NT-GSDMD cardiomyocytes (ACMs) and determine its contribution arrhythmogenesis. Human appendages were used assess protein levels localization. A modified adeno-associated virus 9 was employed establish ACM-restricted overexpression mice. The cleavage GSDMD enhanced ACMs AF patients. Atrial cardiomyocyte-restricted mice increased susceptibility pacing-induced AF. pore formation facilitated interleukin-1β secretion from ACMs, promoting macrophage infiltration, while up-regulating 'endosomal sorting complexes required for transport'-mediated membrane-repair mechanisms, which prevented cell death (pyroptosis) ACMs. Up-regulated directly targeted mitochondria, increasing mitochondrial reactive oxygen species (ROS) generation, triggered proarrhythmic calcium-release events. NT-GSDMD-induced arrhythmogenesis mitigated by mitochondrial-specific antioxidant MitoTEMPO. mutant lacking pore-formation capability failed cause dysfunction or induce arrhythmia. Genetic ablation Gsdmd spontaneous development a mouse model. These findings unique pyroptosis-independent arrhythmogenesis, involves ROS-driven dysfunction. Mitochondrial-targeted therapy, either reducing ROS production inhibition prevents inducibility, positioning as novel therapeutic target prevention.
Language: Английский
Citations
1
Basic Research in Cardiology, Journal Year: 2024, Volume and Issue: 119(2), P. 215 - 242
Published: March 12, 2024
Language: Английский
Citations
8
GeroScience, Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 1, 2024
Language: Английский
Citations
8
Cells, Journal Year: 2024, Volume and Issue: 13(4), P. 311 - 311
Published: Feb. 8, 2024
Atrial fibrillation (AF) is the most common progressive cardiac arrhythmia worldwide and entails serious complications including stroke heart failure. Despite decades of clinical research, current treatment AF suboptimal. This due to a lack knowledge on mechanistic root causes AF. Prevailing theories indicate key role for molecular structural changes in driving electrical conduction abnormalities atria as such triggering Emerging evidence indicates altered atrial systemic immune landscape this so-called electropathology. Immune cells markers play central remodeling by exhibiting dual facets. While activation recruitment contribute maintaining stability, excessive pronounced expression can foster review delineates shifts composition distribution context health disease, especially A comprehensive exploration functions diverse cell types other diseases essential unravel intricacies remodeling. Usltimately, we delve into showcasing modifications both domains among patients, aiming elucidate therapy diagnostics.
Language: Английский
Citations
4
Nature Cardiovascular Research, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 6, 2025
Language: Английский
Citations
0
Heart Rhythm, Journal Year: 2025, Volume and Issue: 22(3), P. 876 - 877
Published: Feb. 27, 2025
Language: Английский
Citations
0
Journal of Molecular and Cellular Cardiology, Journal Year: 2025, Volume and Issue: 202, P. 13 - 23
Published: March 6, 2025
Inflammasomes are multiprotein complexes of the innate immune system that mediate inflammatory responses to infection and local systemic stress tissue injury. The principal function is facilitate caspase-1 auto-activation subsequently maturation release effectors interleukin (IL)-1β IL-18. atrial-specific NLRP3 inflammasome a unifying causal feature atrial fibrillation (AF) development, progression recurrence after ablation. Many AF-associated risk factors co-morbidities converge mechanistically on activation this central signaling platform. This review presents historical conceptual development distinct its potential involvement in AF. We follow early observations linking inflammation with AF, emergence an atrial-intrinsic operating within not just cells but also resident fibroblasts cardiomyocytes. outline key developments understanding how effector IL-1β contribute causally cellular tissue-level arrhythmogenesis different pathological settings, candidate therapeutic concepts verified preclinical models cardiomyopathy
Language: Английский
Citations
0
The Journal of Physiology, Journal Year: 2025, Volume and Issue: unknown
Published: March 7, 2025
Atrial fibrillation (AF) is a complex arrhythmia. Various modulating factors influence its triggers and substrate. Fibroblasts, adipocytes, inflammatory cells the coagulation system can disrupt cardiomyocyte function. Cardiomyocytes fibroblasts release cytokines that promote local systemic inflammation, enhancing fibroblast activation extracellular matrix deposition, leading to myocardial fibrosis. Fibrosis essential for induction of reentrant arrhythmias, including AF. Adipocytes contribute arrhythmogenesis by secreting pro-inflammatory pro-fibrotic factors, exacerbating inflammation metabolic dysregulation. Inflammatory mediators activate system, which augments this vicious cycle producing promoting fibrosis arrhythmias at same time as increasing risk thrombosis. Understanding these interconnected roles in development progress atrial arrhythmogenic substrate may point potential novel therapeutic targets stabilise or antagonise eventually prevent This review examines role interplay between cardiomyocytes, fibroblasts, contributing AF initiation perpetuation.
Language: Английский
Citations
0