[HTML][HTML] ER-mitochondria communication is involved in NLRP3 inflammasome activation under stress conditions in the innate immune system
AC Pereira, J De Pascale, R Resende… - Cellular and Molecular …, 2022 - Springer
Endoplasmic reticulum (ER) stress and mitochondrial dysfunction, which are key events in
the initiation and/or progression of several diseases, are correlated with alterations at ER …
the initiation and/or progression of several diseases, are correlated with alterations at ER …
[PDF][PDF] Endoplasmic reticulum stress activates the inflammasome via NLRP3-and caspase-2-driven mitochondrial damage
Endoplasmic reticulum (ER) stress is observed in many human diseases, often associated
with inflammation. ER stress can trigger inflammation through nucleotide-binding domain …
with inflammation. ER stress can trigger inflammation through nucleotide-binding domain …
[HTML][HTML] Mitochondria fusion upon SERCA inhibition prevents activation of the NLRP3 inflammasome in human monocytes
Sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) is a crucial component of the cellular
machinery responsible for Ca2+ homeostasis. The selective inhibition of SERCA by …
machinery responsible for Ca2+ homeostasis. The selective inhibition of SERCA by …
Mitochondria–endoplasmic reticulum contact sites mediate innate immune responses
T Misawa, M Takahama, T Saitoh - Organelle contact sites: From molecular …, 2017 - Springer
Mitochondria and the endoplasmic reticulum (ER) are fundamental organelles that
coordinate high-order cell functions. Mitochondria are centers of energy production …
coordinate high-order cell functions. Mitochondria are centers of energy production …
Mitochondria: Sovereign of inflammation?
J Tschopp - European journal of immunology, 2011 - Wiley Online Library
NLRP3 inflammasome‐dependent inflammatory responses are triggered by a variety of
signals of host danger, including infection, tissue damage and metabolic dysregulation. How …
signals of host danger, including infection, tissue damage and metabolic dysregulation. How …
[HTML][HTML] Defective mitochondrial fission augments NLRP3 inflammasome activation
Despite the fact that deregulated NLRP3 inflammasome activation contributes to the
pathogenesis of chronic inflammatory or metabolic disorders, the underlying mechanism by …
pathogenesis of chronic inflammatory or metabolic disorders, the underlying mechanism by …
Mitochondria: the indispensable players in innate immunity and guardians of the inflammatory response
A Mohanty, R Tiwari-Pandey, NR Pandey - Journal of cell communication …, 2019 - Springer
Mitochondria, the dynamic organelles and power house of eukaryotic cells function as
metabolic hubs of cells undergoing continuous cycles of fusion and fission. Recent findings …
metabolic hubs of cells undergoing continuous cycles of fusion and fission. Recent findings …
[HTML][HTML] A novel mechanism for NLRP3 inflammasome activation
T Zhang, J Zhao, T Liu, W Cheng, Y Wang, S Ding… - Metabolism Open, 2022 - Elsevier
The NLRP3 inflammasome, as an important component of the innate immune system, plays
vital roles in various metabolic disorders. It has been reported that the NLRP3 …
vital roles in various metabolic disorders. It has been reported that the NLRP3 …
The rOX‐stars of inflammation: links between the inflammasome and mitochondrial meltdown
CL Holley, K Schroder - Clinical & translational immunology, 2020 - Wiley Online Library
The nod‐like receptor protein 3 (NLRP3) inflammasome drives inflammation in response to
mitochondrial dysfunction. As metabolic powerhouses with prokaryotic ancestry …
mitochondrial dysfunction. As metabolic powerhouses with prokaryotic ancestry …
Calcium signaling and mitochondrial destabilization in the triggering of the NLRP3 inflammasome
T Horng - Trends in immunology, 2014 - cell.com
The NLRP3 inflammasome is a cytosolic complex that activates Caspase-1, leading to
maturation of interleukin-1β (IL-1β) and IL-18 and induction of proinflammatory cell death in …
maturation of interleukin-1β (IL-1β) and IL-18 and induction of proinflammatory cell death in …