RESEARCH BRIEF: Novel Therapeutic Protein Identified for the Prevention of Fibrosis
Boston, MA – Chronic kidney disease has reached epidemic proportions in the US, affecting as many as 16 million sufferers. A common underlying characteristic in many diseases, progressive fibrosis can lead to organ failure and death in progressive kidney disease. New research from Brigham and Women’s Hospital (BWH) is the first to identify a therapeutic protein with potential to prevent fibrosis. These findings appear online in Science Translational Medicine.
Fibrosis can occur when the body is repairing damaged tissue or organs. Once damaged tissue is replaced, the process may continue uninhibited, leading normal tissue to be replaced by fibrous scars, which can result in organ failure and death. Fibrosis is a common feature not only in kidney disease, but also in diseases such as cardiac failure, liver cirrhosis, stroke and lung disease.
The researchers found that a therapeutic protein, Serum Amyloid P (SAP), or Pentraxin-2, prevented fibrosis in models of kidney disease. SAP functions only at sites of tissue injury and reprograms inflammatory macrophages, driving the inflammatory and fibrogenic process to become anti-inflammatory, preventing the formation of fibrous scars.
The researchers also determined that kidney fibrosis depends on inflammatory monocytes and macrophages, unlike the heart and lung, which depend on fibrocytes. “This breakthrough in the study of chronic inflammation not only provides a potential new therapy for treatment of chronic diseases,” said Jeremy Duffield, MD, PhD, of the Renal Division at BWH. “It also highlights a key molecular pathway that may be accessible to novel therapeutics in the near future.”
The study was funded by the National Institutes of Health (NIDDK), the American Society of Nephrology, Promedior Inc. and National Taiwan Science Council.
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