For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
63
views
Article has an altmetric score of 1
39
references
 Top references
cited by
5
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      3,311
      similar
       All similar
      • Record: found
      • Abstract: not found
      • Article: not found

      YAP-galectin-3 signaling mediates endothelial dysfunction in angiotensin II-induced hypertension in mice

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" dir="auto" id="d1110559e200">Vascular endothelial dysfunction is regarded as an early event of hypertension. Galectin-3 (Gal-3) is known to participate in various pathological processes. Whilst previous studies showed that inhibition of Gal-3 effectively ameliorates angiotensin II (Ang II)-induced atherosclerosis or hypertension, it remains unclear whether Ang II regulates Gal-3 expression and actions in vascular endothelium. </p>

          Related collections

          Most cited references39

          • Record: found
          • Abstract: found
          • Article: not found

          A role for mitochondria in NLRP3 inflammasome activation.

          Rongbin Zhou, Amir S Yazdi, Philippe Menu … (2011)
          An inflammatory response initiated by the NLRP3 inflammasome is triggered by a variety of situations of host 'danger', including infection and metabolic dysregulation. Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Resting NLRP3 localizes to endoplasmic reticulum structures, whereas on inflammasome activation both NLRP3 and its adaptor ASC redistribute to the perinuclear space where they co-localize with endoplasmic reticulum and mitochondria organelle clusters. Notably, both ROS generation and inflammasome activation are suppressed when mitochondrial activity is dysregulated by inhibition of the voltage-dependent anion channel. This indicates that NLRP3 inflammasome senses mitochondrial dysfunction and may explain the frequent association of mitochondrial damage with inflammatory diseases.
          Article 0 comments Cited 1249 times – based on 0 reviews     Review now
          Article has an altmetric score of 12
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Reactive oxygen species in inflammation and tissue injury.

            Manish Mittal, Mohammad Rizwan Siddiqui, Khiem Vinh Tran … (2014)
            Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
            Article 0 comments Cited 1149 times – based on 0 reviews     Review now
            Article has an altmetric score of 32
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Regulation of the Hippo-YAP pathway by G-protein-coupled receptor signaling.

              Fa-Xing Yu, Bin Zhao, Nattapon Panupinthu … (2012)
              The Hippo pathway is crucial in organ size control, and its dysregulation contributes to tumorigenesis. However, upstream signals that regulate the mammalian Hippo pathway have remained elusive. Here, we report that the Hippo pathway is regulated by G-protein-coupled receptor (GPCR) signaling. Serum-borne lysophosphatidic acid (LPA) and sphingosine 1-phosphophate (S1P) act through G12/13-coupled receptors to inhibit the Hippo pathway kinases Lats1/2, thereby activating YAP and TAZ transcription coactivators, which are oncoproteins repressed by Lats1/2. YAP and TAZ are involved in LPA-induced gene expression, cell migration, and proliferation. In contrast, stimulation of Gs-coupled receptors by glucagon or epinephrine activates Lats1/2 kinase activity, thereby inhibiting YAP function. Thus, GPCR signaling can either activate or inhibit the Hippo-YAP pathway depending on the coupled G protein. Our study identifies extracellular diffusible signals that modulate the Hippo pathway and also establishes the Hippo-YAP pathway as a critical signaling branch downstream of GPCR. Copyright © 2012 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 697 times – based on 0 reviews     Review now
              Article has an altmetric score of 20
                Bookmark
                All references

                Author and article information

                Contributors
                Xiu-Ling Deng: (View ORCID Profile)
                Journal
                Title: Cellular and Molecular Life Sciences
                Abbreviated Title: Cell. Mol. Life Sci.
                Publisher: Springer Science and Business Media LLC
                ISSN (Print): 1420-682X
                ISSN (Electronic): 1420-9071
                Publication date Created: February 2023
                Publication date (Electronic): January 11 2023
                Publication date (Print): February 2023
                Volume: 80
                Issue: 2
                Article
                DOI: 10.1007/s00018-022-04623-5
                PubMed ID: 36629913
                SO-VID: 4220f3f1-85db-4b3b-8a8c-1b79cc8e554e
                Copyright © © 2023
                License:

                https://www.springernature.com/gp/researchers/text-and-data-mining

                https://www.springernature.com/gp/researchers/text-and-data-mining

                History

                Data availability:

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content3,311

                See all similar

                Cited by5

                See all cited by

                Most referenced authors575

                See all reference authors