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Pharmacological inhibition of HSP90 has been shown to protect against inflammatory endothelial barrier dysfunction, in part by disrupting RhoA signaling, suggesting a complex role in regulating microvascular integrity during systemic inflammation (104, 105)

Many authors attributed the increase in tumor volume to the massive drop in apoptosis, which contrasted with dramatic changes in cell cycle with increased proliferation rate [62]

This first-pass mechanism of periportal toxicity for selected compounds, including hepatotoxicants that primarily affect centrilobular hepatocytes, could result from deficient cytoprotective capacity secondary to depletion of phase II conjugating enzymes in addition to being a consequence of a higher exposure gradient to these upstream hepatocytes