Local Inhibition of HSP90 to Prevent Intimal Hyperplasia after Balloon Injury
Abstract
Peripheral arterial disease (PAD) remains a major threat to life and limb and represents a disabling and potentially fatal condition in the aging military and Veteran population. Heat shock protein 90 (HSP90) is a molecular chaperone binds many signaling proteins regulating their final maturation. HSP90 is ubiquitously expressed and is important for normal cell function. However, aberrant activation of HSP90 can result in increased cell migration and proliferation. Inhibition of HSP90 has been in examined in states of aberrant cell growth such as cancer. Our long-term goal is to understand how HSP90 signaling pathways can be manipulated therapeutically to prevent IH in vivo. The objective of this proposal is to investigate the mechanisms by which localized HSP90 inhibition regulate IH development. Our central hypothesis is that localized HSP90 inhibition will effectively inhibit the formation of IH. The rationale for the proposed project is that understanding the underlying mechanisms of dyslipidemia on IH and establishing optimal HSP90 inhibitor delivery to reduce IH will result in novel and innovative approaches to prevent restenosis after angioplasty.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2019
- Accession Number
- AD1095376
Entities
People
- Kristopher Maier