Table 4 Bone diseases or dysfunctions caused by the γ-group of rhodopsin GPCR mutation or deletion

From: The role of GPCRs in bone diseases and dysfunctions

GPCR

Species

Bone diseases or dysfunctions caused by GPCR mutation or deletion

References

BDKRB1

Mouse

Reduced bone loss

Gonçalves et al.190

CCR1

Mouse

Reduced bone mass

Hoshino et al.191

   

Taddei et al.192

CCR2

Human

CCR2 Val/Ile and CCR2 Val+genotype were associated with osteoporosis

Eraltan et al.185

 

Mouse

Delayed fracture healing

Xing et al.199

  

Larger and stronger tibial bones

Mader et al.203

CCR5

Mouse

Reduced cartilage degeneration postsurgery

Takebe et al.204

  

Promoted alveolar bone resorption

Andrade et al.205

CCR6

Mouse

Reduced bone mass

Doucet et al.193

CCR7

Mouse

Reduced functional deficits and subchondral bone changes in the DMM model

Sambamurthy et al.206

CMKLR1

Mouse

Reduced bone mass and BMD in male

Zhao et al.194

CX3CR1

Mouse

Increased bone mass

Hoshino et al.189

CXCR2

Mouse

Reduced body length, bone mass, and BMD

Bischoff et al.36

  

Reduced arthritis severity

Jacobs et al.201

CXCR4

Mouse

Reduced femoral length and bone mass

Zhu et al.195

  

Reduced bone fracture healing

Kawakami et al.200

GPR1

Mouse

Reduced BMD and bone mass

Liet al et al.196

GPR142

Mouse

Reduced CAIA-induced arthritis severity

Murakoshi et al.202

GPR54

Mouse

Reduced bone mass

Brommage et al.197

MCHR1

Mouse

Induced osteoporosis

Bohlooly et al.198

OPRM1

Human

rs9479769, rs4870268, and rs1998221 SNPs were associated with reduced BMD and bone mass

Lu et al.29

  1. BMD bone mineral density, CAIA collagen antibody-induced arthritis, DMM destabilization of the medial meniscus, GPCR G protein-coupled receptor, SNP single-nucleotide polymorphism