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(Circulation Research. 2008;102:270.)
© 2008 American Heart Association, Inc.

Editorials

Novel Role for Osteopontin in Cardiac Fibrosis

Peter Zahradka

From the University of Manitoba and St. Boniface Research Centre, Winnipeg, Canada.

Correspondence to Peter Zahradka, St. Boniface Research Centre, Canadian Centre for Agri-food Research in Health & Medicine, 351 Tache Ave, Winnipeg, MB R2H 2A6, Canada. E-mail peterz@sbrc.ca

See related article, pages 319–327

Key Words: osteopontin • myofibroblast differentiation • HMGB1 • cardiac fibrosis

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Wound healing is a normal physiological process that is required for the repair of tissue damage.¹ The initial stages of this process result in the formation of a scar through deposition of extracellular matrix (ECM) proteins. In the subsequent stages, scar tissue is slowly replaced by new cells. The final result is regeneration of the original tissue and significant restoration of function.

The primary mediator of wound healing is the fibroblast, a nondescript cell found in all tissues.² Activated fibroblasts or myofibroblasts are the source of the ECM proteins that form the scar. Myofibroblasts also help to maintain the integrity of the damaged tissue by contracting the newly deposited ECM, thus promoting wound closure. The scar subsequently serves as a matrix for cell recolonization during tissue regeneration. Accordingly, the scar is a temporary structure that is slowly removed as new cells are produced. Once regeneration is complete, the myofibroblasts revert to their original inactive state.

The interconversion of fibroblasts and myofibroblasts is intended to enable a rapid response to injury while ensuring excessive ECM deposition or fibrotic scarring does not occur. Nevertheless, failure to terminate the wound-healing program, thus leading to persistent activation of fibroblasts, does happen, and is the primary cause of fibrotic disease.^2,3 Because excessive scar production or fibrosis can seriously compromise organ function, there is considerable effort underway to identify methods of preventing this currently untreatable condition.

Unlike most tissues, the heart is unable to repair itself because of the lack of sufficient cardiomyocyte proliferation. Consequently, neither . . . [Full Text of this Article]

Related Article:

Osteopontin Expression Is Required for Myofibroblast Differentiation

Yair Lenga, Adeline Koh, Aruni Shamalee Perera, Christopher A. McCulloch, Jaro Sodek, and Ron Zohar
Circ. Res. 2008 102: 319-327. [Abstract] [Full Text] [PDF]

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