Conflict of Interest The authors have no conflicts of

Conflict of Interest: The authors have no conflicts of interest to declare.
Acknowledgments
Understanding Pulmonary Remodeling The effects of serotonin (5-hydroxytryptamine, 5-HT) class 2 receptors (5-HT2) on airway function and remodeling in respiratory disorders are unclear. Using murine precision-cut lung slices (PCLS) and human bronchial smooth muscle GSK1210151A (HBSMC), Löfdahl et al () studied the role of 5-HT2B receptors in these processes. 5-HT–induced bronchoconstriction in PCLS was studied after preventive treatment with selective 5-HT2 receptor antagonists. A few 5-HT2B receptor antagonists significantly reduced 5-HT–induced bronchoconstriction as well as the release of transforming growth factor (TGF)-β1, a pro-fibrotic growth factor known to enhance airway remodeling. 5-HT–TGF-β1 co-treatment increased HBSMC proliferation, which was reduced by 5-HT2 receptor antagonists. 5-HT2B receptors may mediate pathological pulmonary remodeling.
Characterizing Ovarian Cancer Xenografts The treatment for high-grade serous ovarian cancer (HGSC) is limited by the lack of appropriate cell culture–based models for pre-clinical evaluation. Using gene expression, copy number variation, and exome sequencing analyses, Cybulska et al () molecularly characterized HGSC patient–derived xenografts (PDXs). PDXs mimicked molecular changes observed in analyses of primary human HGSCs and displayed genomic alterations previously identified upon HGSC profiling. PDXs also represented the majority of HGSC subtypes. When mice bearing PDXs were treated with carboplatin, they exhibited similar sensitivity to the drug as the patients' tumors at the time of sampling. HGSC PDXs may help model HGSC preclinically to test potential therapeutics.
GPR40 and GPR84 Regulate Fibrosis Although the G protein–coupled receptors GPR40 and GPR84 are involved in various physiological processes, their role in fibrosis remains unclear. Using mouse models of kidney fibrosis, Gagnon et al () studied the role of GPR40 and GPR84 in fibrosis pathways. Fibrosis was induced by various established methods in transgenic mice lacking Gpr40 or Gpr84. GPR40 was found to be protective and GPR84 deleterious. PBI-4050, a synthetic analog of a medium-chain fatty acid that displays agonist and antagonist ligand affinity toward GPR40 and GPR84, respectively, was administered to these transgenic mice. PBI-4050 bound to GPR40 and GPR84 and significantly reduced fibrosis in various organs. Modulating GPR40 and GPR84 or administering PBI-4050 may help manage inflammation- and fibrosis-related diseases.
Managing Acetaminophen-Induced Liver Injury It is unclear how plasminogen activator inhibitor-1 (PAI-1) averts intrahepatic hemorrhage and mortality after acetaminophen (APAP)-induced liver injury. Pant et al () hypothesized that PAI-1 restricts APAP-induced liver-related injury by decreasing tissue-type plasminogen activator (tPA)-dependent fibrinolysis. Compared to wild type (WT) mice, PAI-1–deficient (PAI-1−/−) mice showed reduced hepatic deposition of cross-linked fibrin, with greater intrahepatic congestion and increased hemorrhage 24 hours after APAP overdose. Administration of recombinant WT human PAI-1 reduced intrahepatic hemorrhage in PAI-1−/− mice. Though tPA deficiency alone had no effect on APAP-induced liver damage, tPA and PAI-1 double-deficient mice showed reduced APAP-induced fibrinolysis, intrahepatic congestion and hemorrhage, as well as mortality. Modulating fibrinolysis may help manage bleeding, thrombosis, pathogenesis of liver injury, and repair of the injured liver after APAP overdose.
Visualizing Proliferative Endothelial Cells Effective drug targeting to tumors is limited by the lack of available tumor endothelial cell (EC) markers. To distinguish dormant and proliferating ECs, Yamakawa et al () generated transgenic mice expressing EGFP under the transcriptional control of the DNA replication factor PSF1/GINS1 promoter. Though dormant ECs in the skin of adult mice lacked EGFP signal, upon subcutaneous injection of tumor cells, proliferating tumor-associated ECs shifted to EGFP-positivity. A few dormant tumor-associated ECs strongly expressed the GPI-anchor protein CD109. Monitoring CD109 expression in tumor vessels may help identify tumor vascular normalization, which facilitates delivery of drugs to the cancers, for effective drug targeting.