Results 101 to 110 of about 10,801 (189)

Diverse Scaffolds Facilitate NLRP3 Clustering and Inflammasome Formation in Response to Perturbations in Cell Homeostasis

BioEssays, Volume 48, Issue 3, March 2026.
NLRP3, a cytosolic innate immune sensor, responds to diverse activators that perturb cellular homeostasis. These disturbances generate molecular scaffolds that, through binding partners such as nucleic acids, lipids, and proteins, recruit and concentrate NLRP3. Scaffold‐mediated NLRP3 clustering promotes NLRP3 inflammasome assembly.
Elvira Boršić‐Mlinarič, Iva Hafner‐Bratkovič   +1 more
wiley   +1 more source

Targeting Autophagy in Ovarian Cancer: The Emerging Role of Ginsenosides

Cancer Medicine, Volume 15, Issue 3, March 2026.
ABSTRACT Background Ovarian cancer, the third most prevalent gynecological malignancy, is frequently diagnosed at an advanced stage owing to its asymptomatic early progression. Despite the application of conventional therapies, clinical management remains limited by adverse effects and the development of drug resistance.
Yuxin Guo, Cuilan Yun, Yuemei Zhang, Xu Yang, Huiqin Liu   +4 more
wiley   +1 more source

Targeting NME3 to Restore Mitochondrial Fission‐Fusion Balance Defines a Novel Disease‐Modifying Strategy for Parkinson's Disease

CNS Neuroscience &Therapeutics, Volume 32, Issue 3, March 2026.
NME3 deficiency disrupts mitochondrial fission‐fusion balance, causing neuronal damage via ROS. Pharmacological Drp1 inhibition (Mdivi‐1) or substantia nigra‐specific NME3 overexpression restores mitochondrial equilibrium, prevents dopaminergic neuron loss, and alleviates motor deficits in PD models.
Chen Qiao, Xiang‐Qi Hu, Shen‐Han Xu, Meng‐Fan Yao, Jun‐Peng Liu, Lei Cao   +5 more
wiley   +1 more source

Müller Glial Kir4.1 Channel Dysfunction in APOE4‐KI Model of Alzheimer's Disease

Glia, Volume 74, Issue 3, March 2026.
APOE4 impairs Müller cell health by reducing Kir4.1 expression and buffering. APOE4 causes mitochondrial dysfunction with decreased ΔΨm and increased ROS. MitoQ restores Kir4.1 expression and reduces ROS in APOE4‐transfected cells. ABSTRACT Alzheimer's disease (AD), particularly late‐onset AD (LOAD), affects millions worldwide, with the apolipoprotein ...
Surabhi D. Abhyankar, Yucheng Xiao, Neha Mahajan, Qianyi Luo, Theodore R. Cummins, Adrian L. Oblak, Bruce T. Lamb, Timothy W. Corson, Ashay D. Bhatwadekar   +8 more
wiley   +1 more source

Structural insights of human mitofusin-2 into mitochondrial fusion and CMT2A onset

Nature Communications, 2019
Mitofusin-2 (MFN2) is a dynamin-like GTPase that plays a central role in regulating mitochondrial fusion and cell metabolism. Here, authors report crystal structures of truncated human MFN2 in different nucleotide-loading states and show that MFN2 forms ...
Yu-Jie Li, Yu-Lu Cao, Jian-Xiong Feng, Yuanbo Qi, Shuxia Meng, Jie-Feng Yang, Ya-Ting Zhong, Sisi Kang, Xiaoxue Chen, Lan Lan, Li Luo, Bing Yu, Shoudeng Chen, David C. Chan, Junjie Hu, Song Gao   +15 more
doaj   +1 more source

Research Trends and Insights of Charcot–Marie–Tooth Disease (CMT): A Visualization Analysis (2000–2025)

Health Science Reports, Volume 9, Issue 3, March 2026.
ABSTRACT Background and Aims The Charcot–Marie–Tooth disease (CMT) comprises genetically diverse motor and sensory neuropathies. This study aims to conduct a comprehensive investigation into the current academic and clinical status of CMT, thereby providing researchers with an extensive understanding of the research landscape and analysis of prevailing
Lanxiao Cao, Yang Liu, Jiaxin Li, Xiaoping Xia, Guohua Zhao   +4 more
wiley   +1 more source

Mutations in PINK1 and Parkin impair ubiquitination of Mitofusins in human fibroblasts.

PLoS ONE, 2011
PINK1 and Parkin mutations cause recessive Parkinson's disease (PD). In Drosophila and SH-SY5Y cells, Parkin is recruited by PINK1 to damaged mitochondria, where it ubiquitinates Mitofusins and consequently promotes mitochondrial fission and mitophagy ...
Aleksandar Rakovic, Anne Grünewald, Jan Kottwitz, Norbert Brüggemann, Peter P Pramstaller, Katja Lohmann, Christine Klein   +6 more
doaj   +1 more source

The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities

MedComm, Volume 7, Issue 3, March 2026.
Diverse diseases converge on NLRP3. We depict a discovery‐to‐clinic track: high‐throughput/phenotypic screens, structure‐guided design, and modality innovation (allosteric inhibitors, interface blockers, degraders) deliver third‐generation, disease‐tailored NLRP3 control.
Chan Zou, Shilong Jiang, Hui Li, Kai Zhao, Dongshen Cao, Guoping Yang   +5 more
wiley   +1 more source

Lidamycin induces mitophagy in pancreatic cancer cells by regulating the expression of Mfn2

Scientific Reports
Lidamycin (LDM) has been confirmed to have a strong anti-pancreatic cancer effect and can affect the mitochondrial function of pancreatic cancer cells. Mitofusin-2 (Mfn2) is located in the outer membrane of mitochondria, and Mfn2 is currently believed to
Boya Wu, Bing Qi, Liumeng Duan, Jing Chen   +3 more
doaj   +1 more source

Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK‐Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome

Cell Proliferation, Volume 59, Issue 3, March 2026.
Pioglitazone suppresses mitochondrial excessive ROS generation and COX‐2 level through inhibition of Drp‐1 mediated mitochondrial fission in an AMPK‐dependent manner in LS. ABSTRACT Loss of function mutations of NDUFS4 resulted in Leigh syndrome, which is a progressive neurodegenerative disease and characterized by mitochondrial oxidative stress ...
Jie Luo, Ling Chen, Xiaoxian Zhang, Qiang Su, Xiaoya Zhou, Qizhou Lian   +5 more
wiley   +1 more source