China
Africa
Explore chapters and articles related to this topic
Embryology, Anatomy, and Physiology of the Adrenal Glands
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Zona fasciculata (ZF)Constitutes up to 75% of the cortex.Secretes mainly cortisol glucocorticoid and some androgen precursors.Cortisol increases in response to stress. Maintains blood pressure (increases the effect of vasoconstrictors).Suppresses the immune system.Increases gluconeogenesis and decreases peripheral glucose uptake.Activates lipolysis.Bone resorption.Skin thinning.
Biochemistry of Exercise Training: Effects on Bone
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Panagiota Klentrou, Rozalia Kouvelioti
Activation (conversion of bone surface area from quiescence to an active state) of bone in the adult skeleton can occur approximately every 10 seconds. In bone resorption, osteoclasts travel to sites of activation via circulation and either Volkmann or Haversian canals for intracortical turnover (35). In trabecular turnover, activation occurs at sites exposed to bone marrow. The time of completion of resorption to the initiation of bone formation at a particular site can take approximately 1 to 2 weeks and is known as the reversal phase. Chemotaxis and certain stimulators of proliferation determine whether osteoblasts will appear at the base of the resorption cavity (35). Bone formation, unlike bone resorption, is a two-step process. First, osteoid is synthesized and laid down at specific sites. Following deposition, osteoblasts begin to mineralize the newly formed protein matrix about 5 to 10 days later (35).
Osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Ippokratis Pountos, Peter V. Giannoudis
Bone is a dynamic organ that constantly undergoes remodeling. Bone remodeling encapsulates two opposing actions: bone resorption and bone formation. These two processes are combined in time and space at the level of basic multicellular units (BMUs). Bone resorption consists of the actions of osteoclasts and involves the dissolution of bone mineral to its components. In immediate succession, osteoblasts synthesize bone matrix and mineralize the previously created void. Various systemic hormones (e.g., parathyroid hormone, vitamin D, steroid hormones) or locally acting cytokines and growth factors regulate the balance between bone resorption and formation. Under physiologic conditions, this process is completed in a period of 3–6 months. Disturbance of this process, with a preponderance of resorption, can lead to osteoporosis.
Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway
Published in Journal of Investigative Surgery, 2023
Shumei Li, Yajie Cui, Min Li, Wenting Zhang, Xiaoxue Sun, Zhaoxu Xin, Jing Li
Bone resorption plays a key role in bone formation. Osteoblasts produce two key cytokines, OPG and RANKL, of which RANKL increases bone resorption by combining with the receptor RANK on osteoblasts, while OPG inhibits its receptor-related binding by binding to RANKL. Thus, an imbalance between the generation of RANKL and OPG determines the rate of bone resorption and maturation. We found a significant increase in the expression of RANKL and a significant decrease in that of OPG in both the Dex-induced OP rat model and osteoblasts exposed to Dex.The findings confirmed that GIOP increased bone resorption and decreased bone maturation. However, the increase in bone resorption was suppressed to some extent by ACT. Previous studies have reported that GC treatment reduces bone formation by increasing the apoptosis of osteoblasts and osteoclasts, which is one of the pathogenic mechanisms of GIOP [33]. We found that Dex-induced apoptosis was significantly increased in osteoblasts, and treatment with ACT inhibited, the apoptosis-promoting effect of Dex. We also found that ACT significantly reduced the Dex-induced decrease in osteoblast viability.
Effects of osthole on osteoporotic rats: a systematic review and meta-analysis
Published in Pharmaceutical Biology, 2022
Bin Wu, Xiu-Fang Zhu, Xiao-Qiang Yang, Wei-Yi Wang, Jian-Hua Lu
Bone remodelling is tightly regulated by bone-forming osteoblasts and bone-resorbing osteoclasts (Kim et al. 2020). When bone resorption is greater than bone formation, there is a net loss of bone tissue (Alippe et al. 2017), which can lead to osteoporosis. Osteoclasts are multinucleated cells derived from monocyte/macrophage lineage and are the only cells capable of bone resorption (Udagawa et al. 2021). The proliferation and differentiation of osteoclasts are regulated by cytokines, transcription factors and osteoclast-related genes such as macrophage-colony stimulating factor and tumour necrosis factor. The OPG/RANKL/RANK pathway is the critically important signalling pathway in the process (Meng et al. 2020). Receptor activator of nuclear factor kappa-Β ligand binds to receptors on the osteoclast surface; it regulates NF-κB signalling, activates nuclear factor of activated T-cells 1, and activates osteoclast-specific molecules (e.g., cathepsin K, matrix metalloproteinase-9, and tartrate-resistant acid phosphatase). Previous in vitro experiments demonstrated that osthole inhibits bone resorption by suppressing proliferation of osteoclasts and expression of osteoclast-specific genes (Zhai et al. 2014; Lv et al. 2016; Ma et al. 2019). The results of this meta-analysis confirmed that osthole had similar effects in vivo, presumably through increased expression of OPG/RANKL (Zhai et al. 2014; Li et al. 2016).
A patent review on cathepsin K inhibitors to treat osteoporosis (2011 – 2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Fernanda R. Rocho, Vinícius Bonatto, Rafael F. Lameiro, Jerônimo Lameira, Andrei Leitão, Carlos A. Montanari
The use of activity-based probes (ABPs) as substrates of CatK has been described in the literature for measuring CatK activity [79–81]. A recent patent [82] presents a series of ‘osteoadsorptive fluorogenic sentinel’ (OFS-1) probes synthesized at the University of Southern California by McKenna CE and shown by Nishimura I (University of California, Los Angeles) to act as substrates of CatK released by osteoclasts. The probe consists of a bone-anchoring bisphosphonate moiety connected to a FRET quencher in a CatK peptide substrate sequence. The fluorogenic substrates are adsorbed by hydroxyapatite (HAp) and bone mineral surfaces, where an external fluorescent signal is generated in response to the osteoclast-secreted CatK. Thus, it is a promising new imaging tool to detect abnormal bone resorption. The resorption can be monitored throughout extended periods with a single dose, differently from existing probes cleared within a few days in vivo.