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@ARTICLE{Hosseini:304505,
      author       = {A. Hosseini and E. Haj-Yehia and S. Korste and Y. Kuzay and
                      M. Trajkovic-Arsic$^*$ and S. Settelmeier and M. Cantore and
                      K. B. Ferenz and J. T. Siveke$^*$ and K. Herrmann and T.
                      Rassaf and U. Hendgen-Cotta and W. A. Weber and Z. Varasteh},
      title        = {{H}ow {R}apidly {D}oes the {FAPI} {PET} {S}ignal {R}everse
                      {F}ollowing {T}herapy? {A}ssessing the {FAPI} {PET} {S}ignal
                      in {H}ypertensive {C}ardiac {I}njury and {F}ibrosis in
                      {M}ice.},
      journal      = {Journal of nuclear medicine},
      volume       = {nn},
      issn         = {0097-9058},
      address      = {New York, NY},
      publisher    = {Soc.},
      reportid     = {DKFZ-2025-01893},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Reactive fibrosis is a complex response to chronic
                      myocardial insults, contributing to heart failure
                      progression. Fibroblast activation protein inhibitor (FAPI)
                      PET shows promise in distinguishing active from established
                      fibrosis. Although antifibrotic therapies may improve left
                      ventricular (LV) function in preclinical studies, their
                      clinical application is limited by the lack of noninvasive
                      imaging methods to assess fibrosis regression. This study
                      investigates the potential of FAPI PET to track the
                      therapeutic transition of activated fibroblast activation
                      protein (FAP)-positive fibroblasts toward a FAP-negative
                      phenotype. Methods: Mice were implanted with minipumps,
                      infused with angiotensin-II/phenylephrine (Ang-II/PE) for 6
                      wk and scanned with 68Ga-FAPI-46 PET/CT longitudinally.
                      Control mice received saline. 68Ga-FAPI-46 biodistribution
                      studies were conducted at preselected time points, and FAPI
                      uptake in the major organs was measured ex vivo. To assess
                      the potential reversibility of the FAPI PET signal in the
                      myocardium and liver, Ang-II/PE infusion was discontinued in
                      a group of animals at 1 and 2 wk, respectively. LV
                      structural and functional changes were assessed via
                      echocardiography, tissue fibrosis via histology, and FAP
                      expression via immunohistochemistry. Results: Significant
                      68Ga-FAPI-46 uptake in the myocardium of treated mice peaked
                      at 1 wk. An increase of 68Ga-FAPI-46 uptake was also
                      observed in the liver, peaking at 2 wk, and decreased
                      significantly at 4 wk. The PET signal declined to an
                      indiscernible level in the heart and liver early after
                      Ang-II/PE withdrawal. Three weeks after the removal of the
                      minipumps, the hearts of mice previously exposed to
                      Ang-II/PE for 1 wk exhibited a significant reduction in
                      fibrosis compared with mice that were sacrificed immediately
                      after 1 wk of Ang-II/PE infusion, without the 3-wk recovery
                      period. Coinjection with excess unlabeled FAPI-46 reduced
                      uptake in the heart, liver, and kidneys. Despite an increase
                      in LV wall thickness at 1 wk, the ejection fraction remained
                      stable initially but dropped significantly by 4 wk.
                      Conclusion: The rapid decline in PET signal after Ang-II/PE
                      withdrawal shows that FAPI PET effectively visualizes
                      dynamic changes in FAP expression, making it a valuable tool
                      for quickly assessing treatment responses targeting
                      activated fibroblasts. The cardiac FAPI signal precedes
                      functional myocardial changes, indicating that FAPI PET
                      could detect early fibrosis in cardiac remodeling leading to
                      heart failure. FAPI PET may also visualize cardiac
                      cirrhosis, a serious complication of cardiac disorders.},
      keywords     = {FAPI PET (Other) / rapid therapy response monitoring
                      (Other) / signal reversibility (Other)},
      cin          = {ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40935615},
      doi          = {10.2967/jnumed.124.268860},
      url          = {https://inrepo02.dkfz.de/record/304505},
}