Results 91 to 100 of about 51,913 (289)

CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis

Advanced Science, EarlyView.
Ferroptosis is driven by mitochondrial permeability transition pore (mPTP) opening, which induces mitochondrial swelling and releases oxidized mitochondrial DNA. The released mtDNA activates cGAS–STING signaling, promotes ferritinophagy, and amplifies ferroptotic cell death. Disruption of mtDNA repair sensitizes tumors to ferroptosis in vivo, revealing
Hong Zhou, Wan Fu, Shizuo Liu, Zili Zhang, Hanyan Luo, Qing Zhong   +5 more
wiley   +1 more source

The Function of Necroptosis and Its Treatment Target in IBD

Mediators of Inflammation
Inflammatory bowel disease (IBD), which encompasses Crohn’s disease (CD) and ulcerative colitis (UC), is a complicated illness whose exact cause is yet unknown.
Francis Atim Akanyibah, Yi Zhu, Tao Jin, Dickson Kofi Wiredu Ocansey, Fei Mao, Wei Qiu   +5 more
doaj   +1 more source

Mitochondrial Protein PGAM5 Regulates Mitophagic Protection against Cell Necroptosis. [PDF]

PLoS ONE, 2016
Necroptosis as a molecular program, rather than simply incidental cell death, was established by elucidating the roles of receptor interacting protein (RIP) kinases 1 and 3, along with their downstream partner, mixed lineage kinase-like domain protein ...
Wei Lu, Junhui Sun, Jeong Seon Yoon, Yan Zhang, Lixin Zheng, Elizabeth Murphy, Mark P Mattson, Michael J Lenardo   +7 more
doaj   +1 more source

RIPK3 restricts viral pathogenesis via cell death-independent neuroinflammation [PDF]

, 2017
Receptor-interacting protein kinase-3 (RIPK3) is an activator of necroptotic cell death, but recent work has implicated additional roles for RIPK3 in inflammatory signaling independent of cell death.
Daniels, Brian P., Gale, Michael, Loo, Yueh-Ming, Martinez, Jennifer, Oberst, Andrew, Oguin III, Thomas H., Olsen, Tayla M., Orozco, Susana, Snyder, Annelise G., Tait, Stephen W.G.   +9 more
core   +1 more source

A Mussel‐Inspired Bioadhesive Patch to Selectively Kill Glioblastoma Cells

Advanced Science, EarlyView.
An innovative mussel‐inspired bioadhesive patch has been developed for post‐surgical glioblastoma treatment. The patch, which adheres strongly in biological environments, releases a localized treatment. This treatment, acting via reactive oxygen species, shows specific toxicity to glioblastoma cells.
Jose Bolaños‐Cardet, Sara Pugliese, Jordi Bruna, Daniel Ruiz‐Molina, Salvio Suárez‐García, Victor J. Yuste   +5 more
wiley   +1 more source

TNF receptor–related factor 3 inactivation promotes the development of intrahepatic cholangiocarcinoma through NF‐κB‐inducing kinase–mediated hepatocyte transdifferentiation

Hepatology, EarlyView., 2022
Abstract Background and Aims Intrahepatic cholangiocarcinoma (ICC) is a deadly but poorly understood disease, and its treatment options are very limited. The aim of this study was to identify the molecular drivers of ICC and search for therapeutic targets.
Yuto Shiode, Takahiro Kodama, Satoshi Shigeno, Kazuhiro Murai, Satoshi Tanaka, Justin Y. Newberg, Jumpei Kondo, Shogo Kobayashi, Ryoko Yamada, Hayato Hikita, Ryotaro Sakamori, Hiroshi Suemizu, Tomohide Tatsumi, Hidetoshi Eguchi, Nancy A. Jenkins, Neal G. Copeland, Tetsuo Takehara   +16 more
wiley   +1 more source

Cleavage of DFNA5 by caspase-3 during apoptosis mediates progression to secondary necrotic/pyroptotic cell death. [PDF]

, 2017
Apoptosis is a genetically regulated cell suicide programme mediated by activation of the effector caspases 3, 6 and 7. If apoptotic cells are not scavenged, they progress to a lytic and inflammatory phase called secondary necrosis.
Alnemri, Diana, Alnemri, Emad S., Cingolani, Gino, Fernandes-Alnemri, Teresa, Mayes, Lindsey, Rogers, Corey   +5 more
core   +2 more sources

An Inflammatory Perspective on Necroptosis [PDF]

Molecular Cell, 2017
Necroptosis (programmed necrosis) occurs in response to TNF, Fas, or TRAIL, as well as certain TLR ligands, when caspase activity required for apoptosis is blocked. Necroptosis is typically considered a highly pro-inflammatory mode of cell death, due to release of intracellular "danger signals" that promote inflammation.
Conor J, Kearney, Seamus J, Martin
openaire   +2 more sources

Homoisoflavanone Delays Colorectal Cancer Progression via DNA Damage‐Induced Mitochondrial Apoptosis and Parthanatos‐Like Cell Death

Advanced Science, EarlyView.
Homoisoflavanone (HIF), a bioactive compound isolated from Polygonatum kingianum, selectively suppresses colorectal cancer progression by inducing DNA damage‐mediated mitochondrial apoptosis and parthanatos‐like cell death. HIF triggers mitochondrial dysfunction, including depolarized membrane potential, elevated ROS, and ATP depletion, while impairing
Hongjie Fan, Huzi Zhao, Pei Zhang, Pengfei Yu, Yunfei Ji, Gang Chen, Hongli Jin, Yanfang Liu, Jin Liu, Zhe‐Sheng Chen, Aiping Lyu, Xinmiao Liang, Yang Chen   +12 more
wiley   +1 more source

Macrophage‐derived MLKL in alcohol‐associated liver disease: Regulation of phagocytosis

Hepatology, EarlyView., 2022
EtOH causes leaky gut allowing bacteria and PAMPs into the liver, resulting in hepatic inflammation and injury. We demonstrate that LPS induces STAT1‐mediated expression and phosphorylation of MLKL in macrophages and identify a novel function that myeloid MLKL translocates to phagosomes and lysosomes and regulates phagocytosis, which contributes to the
Xiaoqin Wu, Xiude Fan, Megan R. McMullen, Tatsunori Miyata, Adam Kim, Vai Pathak, Jianguo Wu, Le Z. Day, Josiah E. Hardesty, Nicole Welch, Jaividhya Dasarathy, Daniela S. Allende, Arthur J. McCullough, Jon M. Jacobs, Daniel M. Rotroff, Srinivasan Dasarathy, Laura E. Nagy   +16 more
wiley   +1 more source