THERAPEUTIC TARGETING OF PARC/CCL18 AND ITS SIGNALING IN PULMONARY FIBROSIS

摘要

The present invention relates to methods of treating, preventing or preventing the progression of fibrosis comprising inhibiting the actions of pulmonary and activation-regulated chemokine (PARC) or at least one of its downstream effector molecules, such as Sp1 transcription factor and protein kinase C-alpha (PKCα). The present invention also relates to methods of screening and/or identifying compounds useful for the treatment of fibrosis comprising contacting PARC or its downstream effector molecules, such as Sp1 or PKCα, with a substance and subsequently determining the effects of the substance on the activity of PARC or Sp1 or PKCα. The present invention also relates to methods of screening and/or identifying compounds that prevent or inhibit collagen deposition comprising contacting PARC or its downstream effector molecules, such as Sp1 or PKCα, with a substance and subsequently determining the effects of the substance on the activity of PARC or Sp1 or PKCα.