TY  - JOUR
A1  - Herrmann, Marietta
A1  - Engelke, Klaus
A1  - Ebert, Regina
A1  - Müller-Deubert, Sigrid
A1  - Rudert, Maximilian
A1  - Ziouti, Fani
A1  - Jundt, Franziska
A1  - Felsenberg, Dieter
A1  - Jakob, Franz
T1  - Interactions between muscle and bone — Where physics meets biology
JF  - Biomolecules
N2  - Muscle and bone interact via physical forces and secreted osteokines and myokines. Physical forces are generated through gravity, locomotion, exercise, and external devices. Cells sense mechanical strain via adhesion molecules and translate it into biochemical responses, modulating the basic mechanisms of cellular biology such as lineage commitment, tissue formation, and maturation. This may result in the initiation of bone formation, muscle hypertrophy, and the enhanced production of extracellular matrix constituents, adhesion molecules, and cytoskeletal elements. Bone and muscle mass, resistance to strain, and the stiffness of matrix, cells, and tissues are enhanced, influencing fracture resistance and muscle power. This propagates a dynamic and continuous reciprocity of physicochemical interaction. Secreted growth and differentiation factors are important effectors of mutual interaction. The acute effects of exercise induce the secretion of exosomes with cargo molecules that are capable of mediating the endocrine effects between muscle, bone, and the organism. Long-term changes induce adaptations of the respective tissue secretome that maintain adequate homeostatic conditions. Lessons from unloading, microgravity, and disuse teach us that gratuitous tissue is removed or reorganized while immobility and inflammation trigger muscle and bone marrow fatty infiltration and propagate degenerative diseases such as sarcopenia and osteoporosis. Ongoing research will certainly find new therapeutic targets for prevention and treatment.
KW  - muscle
KW  - bone
KW  - mechanosensing
KW  - mechanotransduction
KW  - myokines
KW  - osteokines adaptation
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-203399
SN  - 2218-273X
VL  - 10
IS  - 3
ER  - 
TY  - JOUR
A1  - Ziouti, Fani
A1  - Rummler, Maximilian
A1  - Steyn, Beatrice
A1  - Thiele, Tobias
A1  - Seliger, Anne
A1  - Duda, Georg N.
A1  - Bogen, Bjarne
A1  - Willie, Bettina M.
A1  - Jundt, Franziska
T1  - Prevention of bone destruction by mechanical loading is not enhanced by the Bruton's tyrosine kinase inhibitor CC-292 in myeloma bone disease
JF  - International Journal of Molecular Sciences
N2  - Limiting bone resorption and regenerating bone tissue are treatment goals in myeloma bone disease (MMBD). Physical stimuli such as mechanical loading prevent bone destruction and enhance bone mass in the MOPC315.BM.Luc model of MMBD. It is unknown whether treatment with the Bruton's tyrosine kinase inhibitor CC-292 (spebrutinib), which regulates osteoclast differentiation and function, augments the anabolic effect of mechanical loading. CC-292 was administered alone and in combination with axial compressive tibial loading in the MOPC315.BM.Luc model for three weeks. However, neither CC-292 alone nor its use in combination with mechanical loading was more effective in reducing osteolytic bone disease or rescuing bone mass than mechanical stimuli alone, as evidenced by microcomputed tomography (microCT) and histomorphometric analysis. Further studies are needed to investigate novel anti-myeloma and anti-resorptive strategies in combination with physical stimuli to improve treatment of MMBD.
KW  - multiple myeloma
KW  - cancer-induced bone disease
KW  - Bruton's tyrosine kinase inhibitor CC-292
KW  - skeletal mechanobiology
KW  - bone adaptation
KW  - mechanical loading
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-284943
SN  - 1422-0067
VL  - 22
IS  - 8
ER  -