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@ARTICLE{Rehman:866061,
      author       = {Rehman, Michael and Vodret, Simone and Braga, Luca and
                      Guarnaccia, Corrado and Celsi, Fulvio and Rossetti, Giulia
                      and Martinelli, Valentina and Battini, Tiziana and Long,
                      Carlin and Vukusic, Kristina and Kocijan, Tea and Collesi,
                      Chiara and Ring, Nadja and Skoko, Natasa and Giacca, Mauro
                      and Del Sal, Giannino and Confalonieri, Marco and Raspa,
                      Marcello and Marcello, Alessandro and Myers, Michael P. and
                      Crovella, Sergio and Carloni, Paolo and Zacchigna, Serena},
      title        = {{H}igh-throughput screening discovers antifibrotic
                      properties of haloperidol by hindering myofibroblast
                      activation},
      journal      = {JCI insight},
      volume       = {4},
      number       = {8},
      issn         = {2379-3708},
      address      = {Ann Arbor, Michigan},
      publisher    = {JCI Insight},
      reportid     = {FZJ-2019-05301},
      pages        = {e123987},
      year         = {2019},
      abstract     = {Fibrosis is a hallmark in the pathogenesis of various
                      diseases, with very limited therapeutic solutions. A key
                      event in the fibrotic process is the expression of
                      contractile proteins, including α-smooth muscle actin
                      (αSMA) by fibroblasts, which become myofibroblasts. Here,
                      we report the results of a high-throughput screening of a
                      library of approved drugs that led to the discovery of
                      haloperidol, a common antipsychotic drug, as a potent
                      inhibitor of myofibroblast activation. We show that
                      haloperidol exerts its antifibrotic effect on primary murine
                      and human fibroblasts by binding to sigma receptor 1,
                      independent from the canonical transforming growth factor-β
                      signaling pathway. Its mechanism of action involves the
                      modulation of intracellular calcium, with moderate induction
                      of endoplasmic reticulum stress response, which in turn
                      abrogates Notch1 signaling and the consequent expression of
                      its targets, including αSMA. Importantly, haloperidol also
                      reduced the fibrotic burden in 3 different animal models of
                      lung, cardiac, and tumor-associated fibrosis, thus
                      supporting the repurposing of this drug for the treatment of
                      fibrotic conditions.},
      cin          = {IAS-5 / INM-9 / JSC},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121 /
                      I:(DE-Juel1)JSC-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572) / 511 -
                      Computational Science and Mathematical Methods (POF3-511)},
      pid          = {G:(DE-HGF)POF3-572 / G:(DE-HGF)POF3-511},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30996132},
      UT           = {WOS:000465334200005},
      doi          = {10.1172/jci.insight.123987},
      url          = {https://juser.fz-juelich.de/record/866061},
}