scholarly journals KLOTHO, FGF21 AND FGF23: NOVEL PATHWAYS TO MUSCULOSKELETAL HEALTH?

2013 ◽  
pp. 1-5
Author(s):  
B. BARTALI ◽  
R.D. SEMBA ◽  
A.B. ARAUJO

Bone mineral density, muscle mass and physical function reach their peak between the second andfourth decade of life and then decline steadily with aging. The crucial question is: what factors contribute to ormodulate this decline? The aim of this mini-review is to propose a theoretical framework for the potential role ofemerging biomarkers such as klotho, fibroblast growth factors (FGF)21 and FGF23 on musculoskeletal health,with a particular focus on decline in muscle mass and function, and calls for future research to examine thisproposed link. The identification of new physiological mechanisms underlying these declines may open apotentially important avenue for the development of novel intervention strategies aimed at preventing or reducingtheir potentially detrimental consequences.

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 465
Author(s):  
Colleen A. Mangold ◽  
David P. Hughes

Many organisms are able to elicit behavioral change in other organisms. Examples include different microbes (e.g., viruses and fungi), parasites (e.g., hairworms and trematodes), and parasitoid wasps. In most cases, the mechanisms underlying host behavioral change remain relatively unclear. There is a growing body of literature linking alterations in immune signaling with neuron health, communication, and function; however, there is a paucity of data detailing the effects of altered neuroimmune signaling on insect neuron function and how glial cells may contribute toward neuron dysregulation. It is important to consider the potential impacts of altered neuroimmune communication on host behavior and reflect on its potential role as an important tool in the “neuro-engineer” toolkit. In this review, we examine what is known about the relationships between the insect immune and nervous systems. We highlight organisms that are able to influence insect behavior and discuss possible mechanisms of behavioral manipulation, including potentially dysregulated neuroimmune communication. We close by identifying opportunities for integrating research in insect innate immunity, glial cell physiology, and neurobiology in the investigation of behavioral manipulation.


2020 ◽  
Vol 21 (10) ◽  
pp. 1034-1043
Author(s):  
Fatemeh Forouzanfar ◽  
Hamid R. Sadeghnia

Neuropathic pain is caused by a damage to or dysfunction of the somatosensory nervous system. The main mechanisms underlying neuropathic pain include ectopic activity in nociceptive nerves, peripheral and central sensitization, impaired inhibitory modulation, and microglial activation. Fibroblast growth factors (FGFs) make up a large family of growth factors that mediate neural development, metabolism, and function through three main key signaling pathways, including RAS/MAP kinase pathway, PI3 kinase/Akt pathway, and PLCγ. An association between the members of the FGF system and the improvement of neuropathic pain has become evident, recently. These signaling molecules may be expected to provide new drug targets for the treatment of neuropathic pain. To the best of our knowledge, it is the first study that reviews the relationship between some members of the FGF system and neuropathic pain.


2013 ◽  
Vol 219 (1) ◽  
pp. R1-R12 ◽  
Author(s):  
K A Staines ◽  
A S Pollard ◽  
I M McGonnell ◽  
C Farquharson ◽  
A A Pitsillides

Aberrant redeployment of the ‘transient’ events responsible for bone development and postnatal longitudinal growth has been reported in some diseases in what is otherwise inherently ‘stable’ cartilage. Lessons may be learnt from the molecular mechanisms underpinning transient chondrocyte differentiation and function, and their application may better identify disease aetiology. Here, we review the current evidence supporting this possibility. We firstly outline endochondral ossification and the cellular and physiological mechanisms by which it is controlled in the postnatal growth plate. We then compare the biology of these transient cartilaginous structures to the inherently stable articular cartilage. Finally, we highlight specific scenarios in which the redeployment of these embryonic processes may contribute to disease development, with the foresight that deciphering those mechanisms regulating pathological changes and loss of cartilage stability will aid future research into effective disease-modifying therapies.


2021 ◽  
Vol 8 ◽  
Author(s):  
Domenico Azzolino ◽  
Giulia Carla Immacolata Spolidoro ◽  
Edoardo Saporiti ◽  
Costanza Luchetti ◽  
Carlo Agostoni ◽  
...  

Aging is characterized by the progressive decline of muscle mass and function, the so-called sarcopenia. Also bone loss is widespread among older people. Sarcopenia and osteopenia/osteoporosis are associated with several adverse outcomes including falls, risk of fractures, functional decline, frailty, and mortality. Recently, the life-course approach to prevent or delay functional decline has become very popular. Regarding musculoskeletal health, there is suggestive evidence that acting during critical or sensitive periods of life in which each person build-up its biological reserves may influence the rate of functional decline in the later stages of life. A life-course approach to musculoskeletal health should take place during early life when plasticity allows more easily the attainment of the peak of the musculoskeletal system driven by environmental stimuli. The rate of the subsequent decline will depend on the peak previously reached. Nutrition and physical exercise are important environmental factors that can influence musculoskeletal development by favoring and maintaining peak bone and muscle mass and strength. Here we provide an overview of body composition changes occurring across the lifespan and strategies based on nutrition and physical exercise to support musculoskeletal health as well as minimizing losses during older life.


Author(s):  
Alec M. Avey ◽  
Keith Baar

In organisms from flies to mammals, the initial formation of a functional tendon is completely dependent on chemical signals from muscle (myokines). However, how myokines affect the maturation, maintenance, and regeneration of tendons as a function of age is completely unstudied. Here we discuss the role of four myokines - fibroblast growth factors (FGF), myostatin, the secreted protein acidic and rich in cysteine (SPARC), and miR-29 - in tendon development and hypothesize a role for these factors in the progressive changes in tendon structure and function as a result of muscle wasting (disuse, aging and disease). Because of the close relationship between mechanical loading and muscle and tendon regulation, disentangling muscle-tendon crosstalk from simple mechanical loading is experimentally quite difficult. Therefore, we propose an experimental framework that hopefully will be useful in demonstrating muscle-tendon crosstalk in vivo. Though understudied, the promise of a better understanding of muscle-tendon crosstalk is the development of new interventions that will improve tendon development, regeneration, and function throughout the lifespan.


Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 31 ◽  
Author(s):  
Liwei Lang ◽  
Yong Teng

Fibroblast growth factor receptor 4 (FGFR4), a tyrosine kinase receptor for FGFs, is involved in diverse cellular processes, including the regulation of cell proliferation, differentiation, migration, metabolism, and bile acid biosynthesis. High activation of FGFR4 is strongly associated with the amplification of its specific ligand FGF19 in many types of solid tumors and hematologic malignancies, where it acts as an oncogene driving the cancer development and progression. Currently, the development and therapeutic evaluation of FGFR4-specific inhibitors, such as BLU9931 and H3B-6527, in animal models and cancer patients, are paving the way to suppress hyperactive FGFR4 signaling in cancer. This comprehensive review not only covers the recent discoveries in understanding FGFR4 regulation and function in cancer, but also reveals the therapeutic implications and applications regarding emerging anti-FGFR4 agents. Our aim is to pinpoint the potential of FGFR4 as a therapeutic target and identify new avenues for advancing future research in the field.


2010 ◽  
Vol 25 (12) ◽  
pp. 2393-2400 ◽  
Author(s):  
Oliver Fricke ◽  
Ralf Beccard ◽  
Oliver Semler ◽  
Eckhard Schoenau

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