Open Access Article – Potential Role of Rebamipide in Osteoclast Differentiation and Mandibular Condylar Cartilage Homeostasis

Author(s):Takashi Izawa*Islamy Rahma Hutami and Eiji Tanaka

Volume 14, Issue 1, 2018

Page: [62 – 69]

Pages: 8

DOI: 10.2174/1573397113666171017113441

Abstract

Background: Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease that involves changes in subchondral bone and progressive degradation of cartilage. Currently, rebamipide, a gastroprotective drug, is administered to protect gastric mucosa and accelerate ulcer healing.

Objectives: Recent studies have shown that rebamipide also attenuates cartilage degeneration by suppressing oxidative damage and inducing homeostasis of the extracellular matrix of articular chondrocytes. Regarding the latter, reduced expression of cathepsin K, NFATc1, c-Src, and integrin β3, and increased expression of nuclear factor-kappa B, have been found to be mediated by the transcription factor, receptor activator of nuclear factor kappa-B ligand (RANKL).

Methods: Treatment with rebamipide was also found to activate, mitogen-activated protein kinases such as p38, ERK, and JNK to reduce osteoclast differentiation. Taken together, these results strongly indicate that rebamipide mediates inhibitory effects on cartilage degradation and osteoclastogenesis in TMJ-OA.

Results and Conclusion: Here, we highlight recent evidence regarding the potential for rebamipide to affect osteoclast differentiation and TMJ-OA pathogenesis. We also discuss the potential role of rebamipide to serve as a new strategy for the treatment of TMJ-OA. Read now: https://bit.ly/3r05Jso

Editors Choice Article | Mitotherapy as a Novel Therapeutic Strategy for Mitochondrial Diseases

 

Author(s): Ailing Fu*

Graphical Abstract:

 

Abstract:

Background: The mitochondrion is a multi-functional organelle that is mainly responsible for energy supply in the mammalian cells. Over 100 human diseases are attributed to mitochondrial dysfunction. Mitochondrial therapy (mitotherapy) aims to transfer functional exogenous mitochondria into mitochondria-defective cells for recovery of the cell viability and consequently, prevention of the disease progress.

 

Objective: The review summarizes the evidence on exogenous mitochondria that can directly enter mammalian cells for disease therapy following local and intravenous administration, and suggests that when healthy cells donate their mitochondria to damaged cells, the mitochondrial transfer between cells serve as a new mode of cell rescue. Then the transferred mitochondria play their roles in recipient cells, including energy production and maintenance of cell function.
Conclusion: Mitotherapy makes the of modulation of cell survival possible, and it would be a potential therapeutic strategy for mitochondrial diseases.

 

 

 

To read out more, please visit: http://www.eurekaselect.com/175033/article

TESTIMONIAL BY QICAI XIAO!

Qicai Xiao

Contributed Article: “Discovery and Development of Natural Products and their Derivatives as Photosensitizers for Photodynamic Therapy

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