Activation of annexin A1 signalling in renal fibroblasts exerts antifibrotic effects

Neymeyer, Hanna; Labes, Robert; Reverte, Virginia; Sáez, Fara; Stroh, Thomas; Dathe, Christin; Hohberger, Stephan Frank; Zeisberg, Michael; Müller, Gerhard A.; Salazar, Javier; Bachmann, S.; Paliege, Alexander

doi:10.1111/apha.12586

Cited by 43 publications

(45 citation statements)

References 56 publications

(85 reference statements)

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“…The understanding that AnxA1 promotes a resolving phase to counteract the pro-inflammatory response has revealed novel therapeutic applications for AnxA1 to delay or even regress the progression of chronic diseases (Perretti and D'Acquisto, 2009;Neymeyer et al, 2015;Soehnlein, 2015;Rackham et al, 2016). This has become increasingly evident in cardiovascular settings.…”

Section: +mentioning

confidence: 99%

Annexins – insights from knockout mice

Grewal

Wason

Enrich

et al. 2016

Biological Chemistry

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Annexins are a highly conserved protein family that bind to phospholipids in a calcium (Ca 2+ ) -dependent manner. Studies with purified annexins, as well as overexpression and knockdown approaches identified multiple functions predominantly linked to their dynamic and reversible membrane binding behavior. However, most annexins are found at multiple locations and interact with numerous proteins. Furthermore, similar membrane binding characteristics, overlapping localizations and shared interaction partners have complicated identification of their precise functions. To gain insight into annexin function in vivo, mouse models deficient of annexin A1 (AnxA1), A2, A4, A5, A6 and A7 have been generated. Interestingly, with the exception of one study, all mice strains lacking one or even two annexins are viable and develop normally. This suggested redundancy within annexins, but examining these knockout (KO) strains under stress conditions revealed striking phenotypes, identifying underlying mechanisms specific for individual annexins, often supporting Ca 2+ homeostasis and membrane transport as central for annexin biology. Conversely, mice lacking AnxA1 or A2 show extracellular functions relevant in health and disease that appear independent of membrane trafficking or Ca 2+ signaling. This review will summarize the mechanistic insights gained from studies utilizing mouse models lacking members of the annexin family.

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Section: +mentioning

confidence: 99%

Annexins – insights from knockout mice

Grewal

Wason

Enrich

et al. 2016

Biological Chemistry

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“…Furthermore, ANXA1 absence in mice is associated with aggravated bleomycin-induced pulmonary fibrosis (Damazo et al , 2011). Thus, this ligand–receptor interaction may represent a novel therapeutic target to inhibit fibrosis in chronic kidney disease (Neymeyer et al , 2015). The ANXA1 mimetic peptide Ac2-26 also has beneficial effects on lung function and pathology in mice with silicosis suggesting that it could be used as a therapeutic agent in lung disease (Trentin et al , 2015).…”

Section: Externalization Of Annexin A1 - and What Next?mentioning

confidence: 99%

Annexin A1: shifting the balance towards resolution and repair

Leoni

Nusrat²

2016

Biological Chemistry

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“…) and pro‐fibrotic pathways (Neymeyer et al . ). Acute damage is closely related to the primary injury, whereas chronically, there may exist common pathways, such as increased levels of reactive oxygen species, activation of protein kinase C β , up‐regulation of transforming growth factor (TGF)‐ β 1, dysregulation of vascular growth factors (e.g.…”

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confidence: 97%