Results 101 to 110 of about 104,328 (314)

Engineered Exosomal miR‐146a‐5p Reprograms BMSC Fate and Restores Mitochondrial Homeostasis in Glucocorticoid‐Induced Osteonecrosis of Femoral Head

open access: yesAdvanced Science, EarlyView.
Exosomal miR‐146a‐5p is identified as a pivotal regulator in steroid‐induced osteonecrosis. Its reduction activates NF‐κB signaling, compromises mitophagy, and disrupts mitochondrial bioenergetics, resulting in autophagic disequilibrium. Engineered exosomes delivering miR‐146a‐5p reinstate mitochondrial function, augment oxidative phosphorylation and ...
Zehui Lv   +13 more
wiley   +1 more source

Inflammasomes: a novel potential biomarker for chronic heart failure (review)

open access: yesРациональная фармакотерапия в кардиологии
The objective of this review is to analyze publications about biochemical studies of inflammasome profile proteins in patients with heart failure as diagnostic markers and promising therapeutic targets.
Yu. S. Timofeev   +5 more
doaj   +1 more source

Metformin alters signaling induced crosstalk and homeostasis in the carcinogenesis paradigm “Epistemology of the origin of cancer”

open access: yes4 open, 2019
The anti-hyperglycemic drug, Metformin, is effective in treating early stages of diabetes and has been associated with a 37% decrease in cancer incidence. While the precise mechanisms for the anti-cancer effects of Metformin remain to be elucidated, this
Brücher Björn L.D.M., Jamall Ijaz S.
doaj   +1 more source

Nlrp3-/- mice do not exhibit metal-DTH reactivity in vivo or in vitro.

open access: yes, 2019
(A) DTH was determined by measuring paw thickness 48 h after challenge (D 14) in mice that were sensitized and challenged as indicated on D 12 and (B) corresponding representative photographs (correspond to label group numbers 1–4) of inflammatory ...
Lauryn Samelko (424639)   +3 more
core   +1 more source

Leonurine Ameliorates Doxorubicin‐Induced Cardiotoxicity via STING/NF‐κB/NLRP3 Inflammasome Signaling Pathway

open access: yesAdvanced Science, EarlyView.
ABSTRACT Doxorubicin‐induced cardiomyopathy (DIC) remains a dose‐limiting clinical challenge. This study reveals that cardiac vascular endothelial cells (CVECs) act as initial sensors of doxorubicin cardiotoxicity: circulating doxorubicin activates the cGAS‑STING pathway in CVECs, triggering NLRP3 inflammasome‑mediated pyroptosis and release of ...
Wang Jun   +10 more
wiley   +1 more source

1,25-Dihydroxyvitamin D Inhibits Osteoarthritis by Modulating Interaction Between Vitamin D Receptor and NLRP3 in Macrophages [Retraction]

open access: yesJournal of Inflammation Research, 2022
Duan A, Ma Z, Liu W, et al. J Inflamm Res. 2021;14:6523–6542. The Editor and Publisher of Journal of Inflammation Research wish to retract the published article. Concerns were raised following the authors request to replace images from Figure 2 and
Duan A   +10 more
doaj  

ZAP facilitates NLRP3 inflammasome activation via promoting the oligomerization of NLRP3

open access: yesInternational Immunopharmacology
The NOD-like receptor family protein 3 (NLRP3) inflammasome is a crucial complex for the host to establish inflammatory immune responses and plays vital roles in a series of disorders, including Alzheimer's disease and acute peritonitis. However, its regulatory mechanism remains largely unclear.
Danhui Qin   +8 more
openaire   +2 more sources

NLRP3-dependent and -independent processing of interleukin (IL)-1β in active ulcerative colitis

open access: yes, 2019
A contributing factor in the development of ulcerative colitis (UC) and Crohn’s disease (CD) is the disruption of innate and adaptive signaling pathways due to aberrant cytokine production.
Veldhuis, M (15513056)   +6 more
core  

Pathophysiological role and potential drug target of NLRP3 inflammasome in the metabolic disorders

open access: yes
NLRP3 plays a role in the development of autoinflammatory diseases. NLRP3, ASC, and Caspases 1 or 8 make up the NLRP3 inflammasome, which is an important part of innate immune system.
Chen, C, Hu, H, Wang, S
core   +1 more source

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