CaMKK2 Signaling in Metabolism and Skeletal Disease: a New Axis with Therapeutic Potential

Justin N. Williams, Uma Sankar

Research output: Contribution to journalReview article

Abstract

Purpose of Review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to fractures and its regenerative capacity diminishes under such conditions. With a rapidly aging population in the USA and the global increase in diabetes, efficacious, multi-dimensional therapies that can treat or prevent skeletal diseases associated with metabolic dysfunction and inflammatory disorders are acutely needed. Recent Findings: Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a key regulator of nutrient intake, glucose metabolism, insulin production, and adipogenesis. Recent studies suggest a pivotal role for CaMKK2 in bone metabolism, fracture healing, and inflammation. Summary: Aside from rekindling previous concepts of CaMKK2 as a potent regulator of whole-body energy homeostasis, this review emphasizes CaMKK2 as a potential therapeutic target to treat skeletal diseases that underlie metabolic conditions and inflammation.

Original languageEnglish (US)
Pages (from-to)169-177
Number of pages9
JournalCurrent osteoporosis reports
Volume17
Issue number4
DOIs
StatePublished - Aug 15 2019

Keywords

  • CaMKK2
  • Diabetes
  • Diabetic osteopathy
  • Fracture healing
  • Skeletal disease

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

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