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13篇 您的检索式:作者名="Moons Lieve"
    题名 作者 年代 出处 被引量
1Complementary research in mammals and fish indicates MMP-2 as a pleiotropic contributor to optic nerve regeneration显示文摘Matrix metalloproteinases(MMPs)are members of the metzincin superfamily named after the zinc ion and the conserved methionine residue at the active site.In addition to their role in extracellular matrix(ECM)remodeling,these proteinases(in)activate many signaling molecules such as growth factors,adhesion molecules and cytokines;and even exert some intra-Kim Lemmens Inge Van Hove Lieve Moons 2016Neural Regeneration Research2016,11,5:3
2Dendritic shrinkage after injury: a cellular killer or a necessity for axonal regeneration?显示文摘Dendrites form an essential component of the neuronal circuit have been largely overlooked in regenerative research. Nevertheless, subtle changes in the dendritic arbors of neurons are one of the first stages of various neurodegenerative diseases, leading to dysfunctional neuronal networks and ultimately cellular death. Maintaining dendrites is therefore considered an essential neuroprotective strategy. This mini-review aims to discuss an intriguing hypothesis, which postulates that dendritic shrinkage is an important stimulant to boost axonal regeneration, and thus that preserving dendrites might not be the ideal therapeutic method to regain a full functional network upon central nervous system damage. Indeed, our study in zebrafish, a versatile animal model with robust regenerative capacity recently unraveled that dendritic retraction is evoked prior to axonal regrowth after optic nerve injury. Strikingly, inhibiting dendritic pruning upon damage perturbed axonal regeneration. This constraining effect of dendrites on axonal regrowth has sporadically been proposed in literature, as summarized in this short narrative. In addition, the review discusses a plausible underlying mechanism for the observed antagonistic axon-dendrite interplay, which is based on energy restriction inside neurons. Axonal injury indeed leads to a high local energy demand in which efficient axonal energy supply is fundamental to ensure regrowth. At the same time, axonal lesion is known to induce m让ochondrial depolarization, causing energy depletion in the axonal compartment of damaged neurons. Mitochondria, however, become mostly stationary after development, which has been proposed as a potential underlying reason for the low regenerative capacity of adult mammals. Per contra, upon reduced neuronal activity, mitochondrial mobility enhances. In this view, dendritic shrinkage after axonal injury in zebrafish could result in less synaptic input and hence, a release of mitochondria within the soma-dendrite compartment that then translocate to the axonal growth cone to stimulate axonal regeneration. If this hypothesis proofs to be correct, i.e. dendritic remodeling serving as fuel for axonal regeneration, we envision a major shift in the research focus within the neuroregenerative field and in the potential uncovering of various novel therapeutic targets.An Beckers Lieve Moons 2019Neural Regeneration Research2019,14,8:2
3Matrix metalloproteinase‐3 in the central nervous system: a look on the bright side显示文摘Inge Hove Kim Lemmens Sarah Velde Mieke Verslegers Lieve Moons 2012Neurochem2012,,2:1
4Loss of Matrix Metalloproteinase-9 or Matrix Metalloproteinase-12 Protects Apolipoprotein E–Deficient Mice Against Atherosclerotic Media Destruction but Differentially Affects Plaque Growth显示文摘Aernout Luttun Esther Lutgens Ann Manderveld Katleen Maris Désiré Collen Peter Carmeliet Lieve Moons 2004Circulation: Journal of the American Heart Association2004,,11:1
5Revascularization of ischemic tissues by PDGF-CC via effects on endothelial cells and their progenitors显示文摘Li Xuri Tjwa Marc Moons Lieve 2005J Clin Invest2005,115,:1
6Valvular Heart Disease/Pulmonary Hypertension: Inhibition of Tissue Angiotensin-Converting Enzyme With Quinapril Reduces Hypoxic Pulmonary Hypertension and Pulmonary Vascular Remodeling显示文摘Zengxuan Nong Jean-Marie Stassen Lieve Moons Desire Collen Stefan Janssens 1996Circulation1996,,8:1
7Loss of placental growth factor protects mice against vascular permeability in pathological conditions显示文摘Aernout Luttun Koen Brusselmans Hideharu Fukao Marc Tjwa Shigeru Ueshima Jean-Marc Herbert Osamu Matsuo Désiré Collen Peter Carmeliet Lieve Moons 2002Biochemical and Biophysical Research Communications2002,,2:1
8ROCK inhibition as a novel potential strategy for axonal regeneration in optic neuropathies显示文摘Optic neuropathies or optic nerve diseases are a frequent cause of permanent vision loss that can occur after inflammation,ischemia,infection,tumors,trauma and/or an elevated pressure inside the eye(also called intraocular pressure or IOP).Glaucoma or glaucomatous optic neuropathy is the most commonly acquired optic neuropathyInge Van Hove Evy Lefevere Lieve Moons 2015Neural Regeneration Research2015,10,12:1
9Anti-PlGF Inhibits Growth of VEGF(R)-Inhibitor-Resistant Tumors without Affecting Healthy Vessels显示文摘Christian Fischer Bart Jonckx Massimiliano Mazzone Serena Zacchigna Sonja Loges Lucia Pattarini Emmanuel Chorianopoulos Laurens Liesenborghs Marta Koch Maria De Mol Monica Autiero Sabine Wyns Stephane Plaisance Lieve Moons Nico van Rooijen Mauro Giacca Je 2007Cell2007,,:1
10Revascularization of ischemic tissues by PDGF-CC via effects on endothelial cells and their progeni- tors显示文摘Xuri Li Marc Tjwa Lieve Moons 2005J Clin Invest2005,115,:1
11Revascularization of ischemic tissues by PDGF-CC via effects on endothelial cells and their progenitors显示文摘Xuri Li Marc Tjwa Lieve Moons 2005J Clin Invest2005,115,:1
12Reaching for the brain:stimulating neural activity as the big leap in optic nerve regeneration显示文摘In the August issue of Nature Neuroscience,Lim and coworkers reported on their study of axonal regeneration in the adult optic nerve,revealing that combined activation of mammalian target of rapamycin(mTOR)signaling and enhancing neural activity leads to successfulEmiel Geeraerts Lieve Moons Lies De Groef 2016Eye Science2016,31,4:0
13Optic nerve injury-induced regeneration in the adult zebrafish is accompanied by spatiotemporal changes in mitochondrial dynamics显示文摘Axonal regeneration in the central nervous system is an energy-intensive process.In contrast to mammals,adult zebrafish can functionally recover from neuronal injury.This raises the question of how zebrafish can cope with this high energy demand.We previously showed that in adult zebrafish,subjected to an optic nerve crush,an antagonistic axon-dendrite interplay exists wherein the retraction of retinal ganglion cell dendrites is a prerequisite for effective axonal repair.We postulate a‘dendrites for regeneration’paradigm that might be linked to intraneuronal mitochondrial reshuffling,as ganglion cells likely have insufficient resources to maintain dendrites and restore axons simultaneously.Here,we characterized both mitochondrial distribution and mitochondrial dynamics within the different ganglion cell compartments(dendrites,somas,and axons)during the regenerative process.Optic nerve crush resulted in a reduction of mitochondria in the dendrites during dendritic retraction,whereafter enlarged mitochondria appeared in the optic nerve/tract during axonal regrowth.Upon dendritic regrowth in the retina,mitochondrial density inside the retinal dendrites returned to baseline levels.Moreover,a transient increase in mitochondrial fission and biogenesis was observed in retinal ganglion cell somas after optic nerve damage.Taken together,these findings suggest that during optic nerve injury-induced regeneration,mitochondria shift from the dendrites to the axons and back again and that temporary changes in mitochondrial dynamics support axonal and dendritic regrowth after optic nerve crush.An Beckers Luca Masin Annelies Van Dyck Steven Bergmans Sophie Vanhunsel Anyi Zhang Tine Verreet Fabienne EPoulain Karl Farrow Lieve Moons 2023Neural Regeneration Research2023,18,1:0
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