Modulating cell-free DNA biology as the next frontier in liquid biopsies DOI
Shervin Tabrizi, Carmen Martin-Alonso,

Kan Xiong

и другие.

Trends in Cell Biology, Год журнала: 2024, Номер unknown

Опубликована: Дек. 1, 2024

Язык: Английский

The spleen in ischaemic heart disease DOI
Gerd Heusch, Petra Kleinbongard

Nature Reviews Cardiology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 2, 2025

Язык: Английский

Процитировано

6

Trained immunity in chronic inflammatory diseases and cancer DOI
George Hajishengallis, Mihai G. Netea, Triantafyllos Chavakis

и другие.

Nature reviews. Immunology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 31, 2025

Язык: Английский

Процитировано

6

Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders DOI Creative Commons
Guangming Zhang,

Huayuan Wei,

Anliu Zhao

и другие.

Journal of Neuroinflammation, Год журнала: 2025, Номер 22(1)

Опубликована: Фев. 7, 2025

Mitochondrial dysfunction is a pivotal instigator of neuroinflammation, with mitochondrial DNA (mtDNA) leakage as critical intermediary. This review delineates the intricate pathways leading to mtDNA release, which include membrane permeabilization, vesicular trafficking, disruption homeostatic regulation, and abnormalities in dynamics. The escaped activates cytosolic sensors, especially cyclic gmp-amp synthase (cGAS) signalling inflammasome, initiating neuroinflammatory cascades via pathways, exacerbating spectrum neurological pathologies. therapeutic promise targeting discussed detail, underscoring necessity for multifaceted strategy that encompasses preservation homeostasis, prevention leakage, reestablishment dynamics, inhibition activation sensors. Advancing our understanding complex interplay between neuroinflammation imperative developing precision interventions disorders.

Язык: Английский

Процитировано

3

A cis-regulatory element controls expression of histone deacetylase 9 to fine-tune inflammasome-dependent chronic inflammation in atherosclerosis DOI Creative Commons
Yaw Asare,

Guangyao Yan,

Christina Schlegl

и другие.

Immunity, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Common genetic variants in a conserved cis-regulatory element (CRE) at histone deacetylase (HDAC)9 are major risk factor for cardiovascular disease, including stroke and coronary artery disease. Given the consistency of this association its proinflammatory properties, we examined mechanisms whereby HDAC9 regulates vascular inflammation. bound mediated deacetylation NLRP3 NACHT LRR domains leading to inflammasome activation lytic cell death. Targeted deletion critical CRE mice increased Hdac9 expression myeloid cells exacerbate inflammasome-dependent chronic In human carotid endarterectomy samples, was associated with atheroprogression clinical plaque instability. Incorporation TMP195, class IIa HDAC inhibitor, into lipoprotein-based nanoparticles target site myeloid-driven inflammation stabilized atherosclerotic plaques, implying lower rupture events. Our findings link atherogenic provide paradigm anti-inflammatory therapeutics atherosclerosis.

Язык: Английский

Процитировано

2

NINJ1-mediated plasma membrane rupture of pyroptotic endothelial cells exacerbates blood-brain barrier destruction caused by neutrophil extracellular traps in traumatic brain injury DOI Creative Commons

Xiaobo Zheng,

Xue Wang, Sheng-Qing Gao

и другие.

Cell Death Discovery, Год журнала: 2025, Номер 11(1)

Опубликована: Фев. 20, 2025

Abstract Brain endothelial cell (bEC) dysfunction is the main factor of blood-brain barrier (BBB) breakdown, which triggers a vicious cycle aggravating traumatic brain injury (TBI) pathogenesis. Previous studies have revealed that neutrophil extracellular traps (NETs) released by neutrophils can lead to BBB disruption, but there lack research on underlying mechanisms after TBI. Here, excessive NETs were found in both contused tissue and circulation following We could activate TLR4/NF-κB pathway induce bEC pyroptosis, led disruption During this process, ninjurin-1 (NINJ1) was activated pyroptotic bECs, it mediated release high mobility group box 1 protein (HMGB1) via plasma membrane rupture (PMR) promote NET formation. NINJ1-mediated HMGB1 aggravated accumulation forming circle Knockdown NINJ1 rescued formation, attenuated leakage, improved neurological outcomes may represent promising target for alleviating NET-induced destruction other related injuries

Язык: Английский

Процитировано

2

A20 attenuates oxidized self-DNA-mediated inflammation in acute kidney injury DOI Creative Commons
Hanwen Li, Yongyao Wu, Lisha Xiang

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)

Опубликована: Апрель 25, 2025

Abstract The ubiquitin-editing enzyme A20 is known to regulate inflammation and maintain homeostasis, but its role in self-DNA-mediated acute kidney injury (AKI) not well understood. Here, our study demonstrated that oxidized self-DNA accumulates the serum of AKI mice patients. This exacerbates progression by activating cGAS-STING pathway NLRP3 inflammasome. While inhibition STING only slightly attenuates progression, suppression inflammasome-mediated pyroptosis significantly alleviates improves survival mice. Subsequently, we found Tnfaip3 (encoding A20) upregulated following treatment. development dampening signaling NLRP3-mediated pyroptosis. Moreover, A20-derived peptide (P-II) also ox-dsDNA-induced renal Mechanistically, competitively binds with NEK7 thus inhibiting P-II interfere interaction between through Lys140 NEK7. Mutation effects on and/or complex. Conditional knockout macrophages or pharmacological both rescue mouse models. reveals a new mechanism which provides therapeutic strategy for AKI.

Язык: Английский

Процитировано

0

The immunology of stroke and dementia DOI
Costantino Iadecola, Josef Anrather

Immunity, Год журнала: 2025, Номер 58(1), С. 18 - 39

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Exploring neutrophils as therapeutic targets in cardiometabolic diseases DOI
Mattia Albiero, Andrea Baragetti

Trends in Pharmacological Sciences, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Donor-derived Cell-free DNA: A Step Forward in the Quest for Transplant Truth DOI
Philip F. Halloran, Katelynn S. Madill-Thomsen

Transplantation, Год журнала: 2025, Номер unknown

Опубликована: Янв. 28, 2025

Язык: Английский

Процитировано

0

Cell-Free Nucleic Acids for Early Diagnosis of Acute Ischemic Stroke: A Systematic Review and Meta-Analysis DOI Open Access
Xiaodan Zhang, Yuzhou Cai, Brian Sit

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(4), С. 1530 - 1530

Опубликована: Фев. 12, 2025

Rapid identification of acute ischemic stroke (AIS) is challenging in both pre-hospital and hospital settings. We aimed to identify the most promising cell-free nucleic acids (cfNAs) as diagnostic biomarkers for IS within 72 h from symptom onset. searched PubMed, Web Science, EMBASE, Cochrane Library published articles that evaluated blood cfNAs early diagnosis AIS until 10 May 2023. The performances individual were pooled by random-effects meta-analysis based on fold change biomarkers' level between non-AIS patients. Of 2955 records, 66 reporting 143 different met inclusion criteria. median sample size was 110, 21.4% studies performed validation. Among selected high-quality studies, miR-106b-5p, miR-124, miR-155, lncRNA H19, cfDNA showed good performance. Data four involving 355 patients 97 controls meta-analysis, which a significant (pooled ratio 1.48, 95% confidence interval 1.23-1.79, p < 0.001). This review highlights cfDNA, H19 are diagnosis, further research needed verification.

Язык: Английский

Процитировано

0