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1  how they function in normal homeostasis and wound repair.
2 option of a morphogen-responsive function in wound repair.
3 ht temporal regulation crucial for efficient wound repair.
4 catenin at the wound margin during embryonic wound repair.
5 cellular responses are often required during wound repair.
6 dult organisms need efficient strategies for wound repair.
7 gral to tissue development, homeostasis, and wound repair.
8 ll functions, as a key effector of epidermal wound repair.
9 eutic targets for the treatment of defective wound repair.
10 -binding protein Shroom and during embryonic wound repair.
11 lial cells is a central signal driving small wound repair.
12 barrier function, inflammation and efficient wound repair.
13 ch as migration, that play critical roles in wound repair.
14   Active MMP-9 increased alveolar epithelial wound repair.
15 s normally associated with tissue injury and wound repair.
16 ediated mechanism, and this in turn impaired wound repair.
17 an important regulator of corneal epithelial wound repair.
18 tex of the wounded cells contribute to rapid wound repair.
19 ion in human acute wounds, thus accelerating wound repair.
20 obilize fibrocytes, such as inflammation and wound repair.
21 ol and MC2562 were effective in accelerating wound repair.
22 edox signaling pathway that promotes mucosal wound repair.
23  In vivo, lack of NONO resulted in defective wound repair.
24 lls are essential for tissue homeostasis and wound repair.
25 ted in physiological tissue regeneration and wound repair.
26 n, can induce decorin expression and enhance wound repair.
27 atory potential of skin keratinocytes during wound repair.
28 iched for genes involved in inflammation and wound repair.
29 ntified that modify fibrogenesis during skin wound repair.
30  impacts early stages of DETC activation and wound repair.
31 tin, suggesting potential benefit in corneal wound repair.
32 eby facilitating cytoskeletal remodeling and wound repair.
33 , so full induction of Ptgs2 is required for wound repair.
34 terns and events associated with periodontal wound repair.
35 skeletal remodeling processes in single cell wound repair.
36 n was further enhanced in tissues undergoing wound repair.
37 tant protection in terms of host defense and wound repair.
38 cadherin in in vitro restitution and in vivo wound repair.
39 namic process of tissue restructuring during wound repair.
40 wall to prevent blood loss and to facilitate wound repair.
41 rmal T cell (DETC) function during cutaneous wound repair.
42 interfollicular epidermis, as is seen during wound repair.
43 del to dissect the mechanisms of single-cell wound repair.
44 madelta T cells that play important roles in wound repair.
45 ll as in epithelial barrier organization and wound repair.
46 ont of SCs/progeny streaming from HFs during wound repair.
47 s, epithelial-to-mesenchymal transition, and wound repair.
48 6 leads to reduced laminin production during wound repair.
49 r the autograft group at the early stages of wound repair.
50 , regulates Rho and Cdc42 during single-cell wound repair.
51 Depletion of Abr attenuates Rho activity and wound repair.
52 lation of extracellular matrix formation and wound repair.
53 ighly expressed at sites of inflammation and wound repair.
54 important in the control of angiogenesis and wound repair.
55 act additional tumor settings, psoriasis and wound repair.
56 ed their ability to mediate angiogenesis and wound repair.
57  contribute to age-associated alterations in wound repair.
58  myofibroblasts is a key event during normal wound repair.
59 ration, differentiation, immune response and wound repair.
60 e host from invading microbes and to promote wound repair.
61  a key mediator of MSC-driven myocardial and wound repair.
62 to specifically eliminate macrophages during wound repair.
63 lpha activation, inhibiting A2AAR-stimulated wound repair.
64 s of the innate immune response, and prevent wound repair.
65  factor-beta signaling pathway, in cutaneous wound repair.
66  to execute decisions about the direction of wound repair.
67 ranaceus has been reported to promote tissue wound repair.
68 vated during tissue damage to participate in wound repair.
69 gesting that Hoxb13 has a negative effect on wound repair.
70 kely interact with endocrine BMP cues during wound repair.
71 rom prophylactic measures aimed at improving wound repair.
72 -AR for the modulation of corneal epithelial wound repair.
73 he pattern recognition receptor NOD2 in skin wound repair.
74 nce of vascular integrity, angiogenesis, and wound repair.
75 ggesting an active role for this receptor in wound repair.
76 ning excessive proliferation during vascular wound repair.
77 n treatment was analyzed in a mouse model of wound repair.
78 ing embryonic development, reproduction, and wound repair.
79 ver and are active players in cardiovascular wound repair.
80 r cells available for tissue homeostasis and wound repair.
81 and circulating immune cells during vascular wound repair.
82 roxide (H2O2), impaired adenosine stimulated wound repair.
83 that epidermal SIRT1 plays a crucial role in wound repair.
84 -GRN-1, induces angiogenesis and accelerates wound repair.
85 tween macrophages and endogenous MSCs toward wound repair.
86  and resolution of the inflammatory phase of wound repair.
87 hat nerves provide cues essential for timely wound repair.
88 fluences macrophage-mediated inflammation in wound repair.
89 not produce WAE cells and exhibited impaired wound repair.
90 d to inhibition of proliferation and delayed wound repair.
91 were found to exhibit a significant delay in wound repair.
92 eutics for immunological functions including wound repair.
93 epidermal morphogenesis, innate immunity and wound repair.
94 mplicated in angiogenesis, inflammation, and wound repair.
95 ws epithelial remodelling, thus facilitating wound repair.
96 ophages to complex tissue damage signals and wound repair.
97  keratinocytes (KCs) in psoriasis and during wound repair.
98 l cohesion during dynamic processes, such as wound repair.
99 in dissociation of leader cells and impaired wound repair.
100 we propose a role for EDA signaling in adult wound repair.
101 ophages and moderating scar formation during wound repair.
102 onR1 cross-linking and directly promoted ASM wound repair.
103  element required for cell proliferation and wound repair.
104 y elevated levels of cell stress and reduced wound repair.
105 to promote increased epithelial turnover and wound repair.
106  linking innate immune activation to mucosal wound repair.
107 s in peripheral tissue and negatively impact wound repair.
108  further destruction and subsequent delay in wound repair.
109 are important in intercellular signaling and wound repair.
110 ntial role in collagen reorganization during wound repair.
111  tail transection, implicating Mmp9 in acute wound repair.
112 rmacological or genetic approaches disrupted wound repair.
113  fibrosis and promote regenerative cutaneous wound repair.
114  to mobilization of normal stem cells during wound repair.
115 y for actomyosin remodeling during embryonic wound repair.
116 egulated corneal epithelial cell fate during wound repair.
117 ical mediators in the age-related decline in wound-repair.
118 abilizes HIF-1alpha during initial stages of wound repair (1-2 wk); whereas inflammation secondary to
119 de or loss of beta2AR gene deletion promoted wound repair, a finding that is, to our knowledge, previ
120  strong proliferative response that promotes wound repair after colitis.
121 reat corneal inflammation while accelerating wound repair after injury.
122 cellular matrix turnover plays a key role in wound repair after myocardial infarction (MI).
123  mutually exclusive zones during single-cell wound repair and asymmetric cytokinesis, suggesting the
124 tant for TWEAK function during physiological wound repair and disease pathogenesis.
125 controls inflammation and fibroplasia during wound repair and diseases (eg, cancer).
126 tions further distinguish the mechanism from wound repair and dorsal closure.
127 icate Wnt/beta-catenin signaling in abnormal wound repair and fibrogenesis.
128               It is also evident at sites of wound repair and fibrosis, playing a key role in tissue
129 findings support a role for PKCbetaII in IEC wound repair and further demonstrate the ability of epit
130 gulating macrophage-mediated inflammation in wound repair and identify a potential target for the tre
131 fibroblast interactions are important during wound repair and in fibrosis in general, we investigated
132 ently, TLR3 activation was also shown to aid wound repair and increase the expression of genes associ
133 m M1 (inflammatory and antimicrobial) to M2 (wound repair and inflammation resolution) phenotype.
134  in embryogenesis, cell growth and survival, wound repair and inflammation, researchers now aim to de
135 roenvironment and elicit processes common to wound repair and many neoplastic skin disorders.
136 iltration, and tissue injury while improving wound repair and mucosal healing.
137     These results extend the role of Fn14 in wound repair and muscle development to involvement in th
138 ay provide new therapeutic opportunities for wound repair and muscular dystrophies.
139   Bone marrow macrophages stimulate skeletal wound repair and osteoblastic bone formation by poorly d
140 al a potential role for thrombin and PAR1 in wound repair and pathophysiology of the adult heart.
141  and mechanomodulatory approaches to augment wound repair and regeneration.
142 ung injury and that vimentin is required for wound repair and remodeling of the alveolar epithelium.
143 homeostasis by activating genes that promote wound repair and resolve inflammation while repressing g
144 nflammatory response; however, their role in wound repair and scarring is unknown.
145  and lung pathology associated with impaired wound repair and subsequent pulmonary edema.
146  a novel role for Tregs in facilitating skin wound repair and suggest that they use the EGFR pathway
147 o cell adhesion regulation during intestinal wound repair and the development of IBD.
148 of Rho and Cdc42 zones during Xenopus oocyte wound repair and the role played by Abr, a dual guanine
149 ellate cells (HSCs) are critical for hepatic wound repair and tissue remodeling.
150 n, make it a promising substrate for corneal wound repair and tissue-engineering purposes.
151     Villin accumulates in the nucleus during wound repair, and altering the cellular microenvironment
152  keratinocyte growth factors, participate in wound repair, and are necessary for keratinocyte homeost
153 lf-rejuvenation of normal intestinal mucosa, wound repair, and cancer metastasis.
154 Angiogenesis is critical during development, wound repair, and cancer progression.
155 tein expression associated with endocytosis, wound repair, and cancer.
156 y epithelial cell (BEC) barrier function and wound repair, and estrogen differentially regulates IL-6
157 eleasate activates other platelets, promotes wound repair, and initiates inflammatory responses.
158 quired for embryogenesis, morphogenesis, and wound repair, and its Arg-Gly-Asp-containing central cel
159 al cofactor ANKRD1 is sharply induced during wound repair, and its overexpression enhances healing.
160 drives tissue remodeling during development, wound repair, and metastatic invasion.
161 tal importance during embryonic development, wound repair, and pathological conditions such as tumor
162 -1 may compensate for estrogen deficiency in wound repair, and potentially other contexts, is an impo
163                    The roles of other ROS in wound repair are little explored.
164 w this interaction influences the process of wound repair are not well understood.
165  in response to injury, but its functions in wound repair are unknown.
166 mportant factors that can accelerate gastric wound repair as well as contribute to epithelial homeost
167 that can be used as epidermal autografts for wound repair as well as for the delivery of gene therapy
168 ms of corneal epithelial lesions and delayed wound repair, as well as their association with diabetes
169 (HUVECs) in both Boyden chamber and in vitro wound repair assays.
170 re susceptible to DSS, and exhibited delayed wound repair at both the clinical and histologic levels.
171  pDCs in sensing tissue damage and promoting wound repair at skin surfaces.
172      Macrophages are important components of wound repair, both in fending off infection and in coord
173 lls (EPCs) normally augment angiogenesis and wound repair but are functionally impaired in diabetics.
174 rectly promotes mast cell activation and ASM wound repair but indirectly promotes ASM contraction via
175                       They are essential for wound repair, but also interfere with axonal regrowth.
176 ay important roles in tissue homeostasis and wound repair, but their role in UV radiation (UVR)-media
177 the role of humoral factors in modulating db wound repair by generating chimeric animals through para
178 nate cells necessary for pathogen control or wound repair can occur without recruitment of potentiall
179   Collective cell migration is a hallmark of wound repair, cancer invasion and metastasis, immune res
180        Myofibroblasts are a key cell type in wound repair, cardiovascular disease, and fibrosis and i
181 vestment in one aspect of personal immunity (wound repair) causes a temporary decrease in one aspect
182 lls, and these ANXA1-containing EVs activate wound repair circuits.
183 ion represents a major mechanism of vascular wound repair, constituting a relevant target and mechani
184                   16 patients needed primary wound repair due to the leakage in insertion sites befor
185                                       During wound repair, epidermal cells at the edge of an injury e
186 ns (e.g., drug delivery, tissue engineering, wound repair, etc.) through judicious selection of the m
187  in normal intestinal homeostasis and during wound repair following mucosal injury.
188 ptional program is critical during cutaneous wound repair for the regulation of scar size; however, t
189 appaB pathway in the localized activation of wound repair genes around epidermal breaks.
190  identify microRNAs negatively impacting the wound repair, global miRNA profiling of wounds collected
191 n outside their niche, either in vitro or in wound-repair, hair follicle stem cells dynamically remod
192           Thus, in addition to their role in wound repair, HFs can make a significant contribution to
193 r of innate physiologic processes, including wound repair, immune response, coagulation and complemen
194 1alpha mutant construct inhibited epithelial wound repair, implicating HIF-1alpha in NO-mediated inhi
195 provides a unique ex vivo model for studying wound repair in a clinically relevant setting.
196 the contribution of hypoxia to mechanisms of wound repair in a model of the intestinal submucosa.
197 tial stem cell niche component that promotes wound repair in adipose, muscle, and lung tissues.
198 how that locally administered IGF-1 promotes wound repair in an estrogen-deprived animal model, the o
199 tin is required and sufficient for increased wound repair in an in vitro model of lung injury.
200 d the influence of 17beta-estradiol on acute wound repair in castrated male mice.
201  role for circulating factors in normalizing wound repair in diabetes.
202 ction of medial actomyosin structures during wound repair in early embryos involves disassembly of th
203                               The process of wound repair in epithelium-lined organs of mammals is co
204 vel therapeutic target to enhance intestinal wound repair in inflammatory bowel diseases.
205           Here we demonstrated that vascular wound repair in KIS(-/-) mice resulted in accelerated fo
206           Here we demonstrated that vascular wound repair in KIS-/- mice resulted in accelerated form
207  either intracellular Ca(2+) mobilization or wound repair in living tissues.
208 the complex, multireceptor-driven process of wound repair in mice in a GEF-dependent manner.
209 ronment on primary keratinocyte function and wound repair in mice.
210 ronment on primary keratinocyte function and wound repair in mice.
211 , apocrine glands, and sebaceous glands) for wound repair in model animals, the present study was des
212 actin and myosin dynamics during single-cell wound repair in the Drosophila embryo.
213 --contributes to the increased efficiency of wound repair in the early embryo.
214 pha1 in Ca(2+) influx-mediated signaling and wound repair in the endothelium.
215 te the mechanisms of force generation during wound repair in the epidermis of early and late Drosophi
216 he cytoskeleton machinery during single cell wound repair in the genetically amenable Drosophila embr
217 e stem cells maintain normal homeostasis and wound repair in the skin is particularly important, as t
218 nment, yet the signaling pathways initiating wound repair in vivo remain little understood.
219 interactions using DETC TCR tetramers delays wound repair in vivo, highlighting DETC as rapid respond
220 ithelialized faster in the first few days of wound repair in vivo.
221 t to recombinant CD44 or TLR2,4, and altered wound repair in wild-type but not RHAMM(-/-) mice.
222 istic of Type 2 immunity (e.g., fibrosis and wound repair) in Chlamydia-infected tissue.
223 TPase activity were analyzed during cellular wound repair, in which arrays close in association with
224 ilencing of Doux-1 improved the rate of cell wound repair induced by CSE treatment.
225 RN, or progranulin) is a protein involved in wound repair, inflammation, and neoplasia.
226  under many physiological conditions such as wound repair, inflammation, and thrombotic reactions and
227            Progranulin (PGRN) is involved in wound repair, inflammation, and tumor formation, but its
228 itical step of normal embryonic development, wound repair, inflammatory response, and tumor cell meta
229             Epithelial cell migration during wound repair involves a complex interplay of intracellul
230                                              Wound repair is a fundamental, conserved mechanism for m
231                                              Wound repair is a key feature distinguishing living from
232                   Thus, in zebrafish larvae, wound repair is driven by an autoregulatory circuit that
233                                    Embryonic wound repair is driven by the evolutionary conserved red
234  versus pathogenic microbial interactions in wound repair is important.
235  Understanding growth factor function during wound repair is necessary for the development of therape
236 tworks in generating mechanical force during wound repair is not well understood.
237                                              Wound repair is often associated with an accumulation of
238 etermining the variable outcome of mammalian wound repair, little is known about the modulation of im
239  ERK, or JNK pathways alone fail to activate wound repair loci.
240                 As such, cells have a robust wound repair mechanism comprised of dynamic membrane res
241 such as cell migration during development or wound repair, mitotic cell detachment, and physiological
242 ine stimulation was evaluated in an in vitro wound repair model and T cell-mediated cytotoxicity expe
243 how that in the Drosophila melanogaster cell wound repair model Rho GTPase arrays form in response to
244                In a model of excisional skin wound repair, Nbeal2-deficient mice exhibited impaired d
245  microvesicles and exosomes; plasma membrane wound repair; neuron pruning; extraction of defective nu
246                              Such defects in wound repair occur in transplant recipients treated with
247 r Tcf3 and Tcf4 in long-term maintenance and wound repair of both epidermis and hair follicles, sugge
248 oV pathogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth
249 ge-activated signaling pathways to promote a wound repair phenotype.
250 tion to their pivotal role in thrombosis and wound repair, platelets participate in inflammatory resp
251 upregulated during the inflammatory phase of wound repair, predominantly expressed in epidermal kerat
252                         In human adults, the wound repair process commonly leads to a non-functioning
253               Fibrogenesis is a pathological wound repair process that fails to cease, even when the
254 ood that endogenous IGF-1 is involved in the wound repair process, the effects of exogenous IGF-1 adm
255 le containing byproducts associated with the wound repair process.
256 re involved in virtually every aspect of the wound repair process; however, the impact of commensal m
257 demonstrate that STING signaling facilitates wound repair processes and that analogous to MyD88-defic
258                  beta2AR antagonism promoted wound repair processes in the early stages of wound repa
259 says were used to assess calcium signalling, wound repair, proliferation, apoptosis and contraction.
260 key ligand in the CXCR3 signaling system for wound repair, promoting re-epithelialization and modulat
261 effects of exogenous IGF-1 administration on wound repair remain largely unclear.
262 n implicated in both conditions, its role in wound repair remains unclear.
263                 Thrombin plays a key role in wound repair, remodeling, and fibrosis after injury and
264                                         Skin wound repair requires a coordinated program of epithelia
265                                         Skin wound repair requires complex and highly coordinated int
266            Our results show that single-cell wound repair requires specific spatial and temporal cyto
267                               The process of wound repair requires the coordinated participation of m
268                          Efficient cutaneous wound repair requires the migration of cells at the woun
269 the body's innate immune response and during wound repair, respectively.
270                                     The cell wound repair response is an example of how specific path
271 and human skin and is an important part of a wound repair response.
272 ound repair processes in the early stages of wound repair, revealing a possible new avenue for therap
273 ut wounding methods has hindered single-cell wound repair studies.
274 ins upregulated at sites of inflammation and wound repair, synergize with FasL to induce apoptosis by
275                         One key component of wound repair that is often overlooked is mechanical forc
276 idelity" recreates a state akin to transient wound repair that persists to maintain uncontrolled grow
277 nd Lpar1(-/-) mice display defective mucosal wound repair that requires cell proliferation and migrat
278 the role of each cell type in the process of wound repair, the nature of the dynamic interplay betwee
279 efficient fibrin clearance can impede normal wound repair, the precise contribution of fibrin to bone
280  cells contribute to tissue regeneration and wound repair through cellular programs that can be hijac
281 h proteoglycan, mediates scarless fetal skin wound repair through, in part, transforming growth facto
282  conditions including embryonic development, wound repair, tumor growth and metastasis.
283                   Unfortunately for mammals, wound repair typically results in scarring and nonfuncti
284 rly stages of skin development and modulates wound repair upon injury.
285 ked whether TLR9 is important for intestinal wound repair using a dextran sulfate sodium (DSS)-induce
286 udy, we evaluate the dynamics of periodontal wound repair using micro-computed tomography (microCT) a
287               Ptgs2(-/-) mice had defects in wound repair, validating the biopsy technique as a syste
288 ent lipid signaling that facilitates mucosal wound repair via spatial targeting of distinct PLC-betas
289  are also potentially important mediators of wound repair via the production of glycosaminoglycan com
290                                      Uterine wound repair was studied by using two strains of mice wi
291 tification, keratinocyte differentiation and wound repair, was increased, whereas the Hh pathway was
292  show that lineage plasticity is critical in wound repair, where it operates transiently to redirect
293 cal treatment of mice with TIP39 accelerated wound repair, whereas TIP39-deficient mice had delayed r
294 fundamental mechanisms of fetal regenerative wound repair, which has the potential to provide insight
295 rmation, and decreased endothelial monolayer wound repair, which was prevented by PEG-SOD and NO dono
296 e demonstrated defects in intestinal mucosal wound repair, while systemic administration of ANXA1 pro
297 ng, including the transcriptional control of wound repair, will be important for the development of f
298             Acute and focal injuries trigger wound repair with tissue replacement.
299 ution of macrophages to helminth killing and wound repair, with specific attention paid to distinct c
300 ncer cell lines increased cell migration and wound repair without affecting cell growth.

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