αKLOTHO and sTGFβR2 treatment counteract the osteoarthritic phenotype developed in a rat model

Publicado en: Protein Cell

Martinez-Redondo, P., Guillen-Guillen, I., Davidsohn, N. et al. αKLOTHO and sTGFβR2 treatment counteract the osteoarthritic phenotype developed in a rat model. Protein Cell

Homeostasis and repair are critical biological processes that allow for tissue and organ preservation and function in multi-cellular organisms. Their regulation and extension vary drastically across the animal kingdom, and mammals show limited tissue-specific regenerative capacity that declines with age. During aging, articular cartilage is one of the tissues that undergo substantial changes in the matrix structure, molecular composition, metabolic activity, and mechanical properties (Loeser et al. 2016). As a result, articular cartilage experiences impaired homeostasis and limited capacity to undergo repair, contributing to osteoarthritis (OA) development (Loeser et al. 2016). OA is the most prevalent musculoskeletal disorder among the elderly and is the leading cause of disability in the US due to pain associated with the disease (Zhang et al. 2016). Although symptomatic pain relief is possible (Zhang et al. 2016), treatments to cure the pathology are currently unavailable. Interestingly, contrary to the loss of homeostasis and repair capacity with age, during embryogenesis as well as a short period after birth, mammals seem to have a higher regeneration capacity (Vivien et al. 2016). These and other facts beg the question of whether therapeutic targets can be developed towards the enhancement of the low regenerative capacity observed during adulthood and worsen upon aging.


Paloma Martinez-Redondo, Isabel Guillen-Guillen, Chao Wang, Javier Prieto, Masakazu Kurita, Fumiyuki Hatanaka, Cuiqing Zhong, Reyna Hernandez-Benitez, Tomoaki Hishida, Takashi Lezaki, Akihisa Sakamoto, Amy N. Nemeth, Yuriko Hishida, Concepcion Rodriguez Esteban, Kensaku Shojima, Pradeep Reddy & Juan Carlos Izpisua Belmonte


Paloma Martinez-Redondo and Isabel Guillen-Guillen have contributed equally to this work.



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