Results 41 to 50 of about 10,801 (189)

MitoSwap – Mitophagy partnered with compensatory mitochondrial biogenesis during stem cell differentiation

Autophagy Reports, 2022
Differentiating stem cells must adapt their mitochondrial metabolism to fit the needs of the mature differentiated cell. In a recent study, we observed that during differentiation to an endothelial phenotype, pluripotent stem cell mitochondria are ...
Priyanka Gajwani, Jalees Rehman
doaj   +1 more source

Mitofusin 2 Deficiency Causes Pro-Inflammatory Effects in Human Primary Macrophages

Frontiers in Immunology, 2021
Mitofusin 2 (MFN2) is a mitochondrial outer membrane GTPase, which modulates mitochondrial fusion and affects the interaction between endoplasmic reticulum and mitochondria.
Vera Khodzhaeva, Yannick Schreiber, Gerd Geisslinger, Gerd Geisslinger, Ralf P. Brandes, Bernhard Brüne, Bernhard Brüne, Bernhard Brüne, Bernhard Brüne, Dmitry Namgaladze   +9 more
doaj   +1 more source

Mitofusin-2 regulates leukocyte adhesion and β2 integrin activation. [PDF]

J Leukoc Biol, 2022
AbstractNeutrophils are critical for inflammation and innate immunity, and their adhesion to vascular endothelium is a crucial step in neutrophil recruitment. Mitofusin-2 (MFN2) is required for neutrophil adhesion, but molecular details are unclear. Here, we demonstrated that β2-integrin-mediated slow-rolling and arrest, but not PSGL-1-mediated cell ...
Liu W, Hsu AY, Wang Y, Lin T, Sun H, Pachter JS, Groisman A, Imperioli M, Yungher FW, Hu L, Wang P, Deng Q, Fan Z.   +12 more
europepmc   +3 more sources

Mitofusin 2 Inhibits Angiotensin II-Induced Myocardial Hypertrophy

Journal of Cardiovascular Pharmacology and Therapeutics, 2010
Background and Objectives: Myocardial hypertrophy is a common clinical finding leading to heart failure and sudden death. Mitofusin 2 (Mfn2), a hyperplasia suppressor protein, is downregulated in hypertrophic heart. This study examined the role of Mfn2 in myocardial hypertrophy and its potential signal pathway. Methods and Results: In in vitro studies,
Haiyi, Yu, Yanhong, Guo, Lin, Mi, Xueying, Wang, Lei, Li, Wei, Gao   +5 more
openaire   +2 more sources

Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction

Neural Regeneration Research
Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment. However, little is known about how fibrosis is induced and regulated after cerebral ischemic injury.
Jun Wen, Hao Tang, Mingfen Tian, Ling Wang, Qinghuan Yang, Yong Zhao, Xuemei Li, Yu Ren, Jiani Wang, Li Zhou, Yongjun Tan, Haiyun Wu, Xinrui Cai, Yilin Wang, Hui Cao, Jianfeng Xu, Qin Yang   +16 more
doaj   +1 more source

Mice Hemizygous for a Pathogenic Mitofusin-2 Allele Exhibit Hind Limb/Foot Gait Deficits and Phenotypic Perturbations in Nerve and Muscle. [PDF]

PLoS ONE, 2016
Charcot-Marie-Tooth disease type 2A (CMT2A), the most common axonal form of hereditary sensory motor neuropathy, is caused by mutations of mitofusin-2 (MFN2). Mitofusin-2 is a GTPase required for fusion of mitochondrial outer membranes, repair of damaged
Peter Bannerman, Travis Burns, Jie Xu, Laird Miers, David Pleasure   +4 more
doaj   +1 more source

Mitofusin-2 is required for mouse oocyte meiotic maturation [PDF]

Scientific Reports, 2016
AbstractMitofusin-2 (Mfn2) is essential for embryonic development, anti-apoptotic events, protection against free radical-induced lesions and mitochondrial fusion in many cells. However, little is known about its mechanism and function during oocyte maturation.
Jing-Hua Zhang, Teng Zhang, Si-Hua Gao, Ke Wang, Xiu-Yan Yang, Fang-Fang Mo, Na Yu, Tian An, Yu-Feng Li, Ji-Wei Hu, Guang-Jian Jiang   +10 more
openaire   +2 more sources

Chloroplast Stress Signals Orchestrate Epidermis‐Specific Remodeling of Mitochondria and ER Under High Light

Advanced Science, EarlyView.
High light exposure triggers an epidermis‐specific remodeling of mitochondria and ER in Arabidopsis, driven by chloroplast‐derived signals. Live‐cell imaging shows that HL rapidly suppresses mitochondrial motility, followed by fusion‐driven elongation and ER cisternal expansion.
Evan R. Angelos, Hee‐Seung Choi, Jingzhe Guo, Andrea A. Zanini, Tessa M. Burch‐Smith, Emily Snyder, Matthew Part, Wilhelmina van de Ven, Manhoi Hur, Gerd Ulrich Balcke, Alain Tissier, Quanqing Zhang, Katayoon Dehesh   +12 more
wiley   +1 more source

Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy [PDF]

Human Molecular Genetics, 2010
Mitochondrial dysfunction and perturbed degradation of proteins have been implicated in Parkinson's disease (PD) pathogenesis. Mutations in the Parkin and PINK1 genes are a cause of familial PD. PINK1 is a putative kinase associated with mitochondria, and loss of PINK1 expression leads to mitochondrial dysfunction, which increases with time.
Matthew E, Gegg, J Mark, Cooper, Kai-Yin, Chau, Manuel, Rojo, Anthony H V, Schapira, Jan-Willem, Taanman   +5 more
openaire   +2 more sources

Astrocytic Mitochondria Transplantation Rescues Neuron Loss and Dendritic Injuries in Acute Cerebral Ischemic Stroke Mouse Model by Flexibly Regulating Mitochondria Dynamics

Annals of Neurology, EarlyView.
Objective Cerebral ischemic stroke causes neuronal oxygen/energy deprivation, disrupting mitochondrial function including reduced membrane potential and bioenergetics, exacerbating neuronal injury. Mitochondrial defects are, therefore, a central neuropathological node and potential therapeutic target.
Ning Bian, Jianing Shen, Linwei Tian, Jinghui Li, Lu Yang, Bo Yuan, Shulin Li, Yuyu Niu, Lu Zhao, Jingkuan Wei   +9 more
wiley   +1 more source