Contribution of Reactive Oxygen Species to Cartilage Degradation in Rheumatic Diseases: Molecular Pathways, Diagnosis and Potential Therapeutic Strategies

2003 ◽  
Vol 10 (20) ◽  
pp. 2123-2145 ◽  
Author(s):  
J. Schiller ◽  
B. Fuchs ◽  
J. Arnhold ◽  
K. Arnold
2007 ◽  
Vol 9 (10) ◽  
pp. 1541-1568 ◽  
Author(s):  
Kyra A. Gelderman ◽  
Malin Hultqvist ◽  
Lina M. Olsson ◽  
Kristin Bauer ◽  
Angela Pizzolla ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2382
Author(s):  
Sepideh Mirzaei ◽  
Kiavash Hushmandi ◽  
Amirhossein Zabolian ◽  
Hossein Saleki ◽  
Seyed Mohammad Reza Torabi ◽  
...  

The failure of chemotherapy is a major challenge nowadays, and in order to ensure effective treatment of cancer patients, it is of great importance to reveal the molecular pathways and mechanisms involved in chemoresistance. Cisplatin (CP) is a platinum-containing drug with anti-tumor activity against different cancers in both pre-clinical and clinical studies. However, drug resistance has restricted its potential in the treatment of cancer patients. CP can promote levels of free radicals, particularly reactive oxygen species (ROS) to induce cell death. Due to the double-edged sword role of ROS in cancer as a pro-survival or pro-death mechanism, ROS can result in CP resistance. In the present review, association of ROS with CP sensitivity/resistance is discussed, and in particular, how molecular pathways, both upstream and downstream targets, can affect the response of cancer cells to CP chemotherapy. Furthermore, anti-tumor compounds, such as curcumin, emodin, chloroquine that regulate ROS and related molecular pathways in increasing CP sensitivity are described. Nanoparticles can provide co-delivery of CP with anti-tumor agents and by mediating photodynamic therapy, and induce ROS overgeneration to trigger CP sensitivity. Genetic tools, such as small interfering RNA (siRNA) can down-regulate molecular pathways such as HIF-1α and Nrf2 to promote ROS levels, leading to CP sensitivity. Considering the relationship between ROS and CP chemotherapy, and translating these findings to clinic can pave the way for effective treatment of cancer patients.


RSC Advances ◽  
2016 ◽  
Vol 6 (60) ◽  
pp. 55092-55103 ◽  
Author(s):  
Md. Maroof Alam ◽  
K. M. Abdullah ◽  
Braj Raj Singh ◽  
Alim Hussain Naqvi ◽  
Imrana Naseem

Quercetin is a natural polyphenolic compound that acts as a strong antioxidant for reactive oxygen species (ROS) generated by any physical or chemical action.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hyunyun Kim ◽  
Jisoo Yun ◽  
Sang-Mo Kwon

Accumulating evidence indicates that acute and chronic uncontrolled overproduction of oxidative stress-related factors including reactive oxygen species (ROS) causes cardiovascular diseases (CVDs), atherosclerosis, and diabetes. Moreover ROS mediate various signaling pathways underlying vascular inflammation in ischemic tissues. With respect to stem cell-based therapy, several studies clearly indicate that modulating antioxidant production at cellular levels enhances stem/progenitor cell functionalities, including proliferation, long-term survival in ischemic tissues, and complete differentiation of transplanted cells into mature vascular cells. Recently emerging therapeutic strategies involving adult stem cells, including endothelial progenitor cells (EPCs), for treating ischemic CVDs have highlighted the need to control intracellular ROS production, because it critically affects the replicative senescence ofex vivoexpanded therapeutic cells. Better understanding of the complexity of cellular ROS in stem cell biology might improve cell survival in ischemic tissues and enhance the regenerative potentials of transplanted stem/progenitor cells. In this review, we will discuss the nature and sources of ROS, drug-based therapeutic strategies for scavenging ROS, and EPC based therapeutic strategies for treating oxidative stress-related CVDs. Furthermore, we will discuss whether primed EPCs pretreated with natural ROS-scavenging compounds are crucial and promising therapeutic strategies for vascular repair.


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jolie Kiemlian Kwee

Modulation of intracellular antioxidant concentration is a double-edged sword, with both sides exploited for potential therapeutic benefits. While antioxidants may hamper the efficacy of chemotherapy by scavenging reactive oxygen species and free radicals, it is also possible that antioxidants alleviate unwanted chemotherapy-induced toxicity, thus allowing for increased chemotherapy doses. Under normoxic environment, antioxidants neutralize toxic oxidants, such as reactive oxygen species (ROS), maintaining them within narrow boundaries level. This redox balance is achieved by various scavenging systems such as enzymatic system (e.g., superoxide dismutases, catalase, and peroxiredoxins), nonenzymatic systems (e.g., glutathione, cysteine, and thioredoxin), and metal-binding proteins (e.g., ferritin, metallothionein, and ceruloplasmin) that sequester prooxidant metals inhibiting their participation in redox reactions. On the other hand, therapeutic strategies that promote oxidative stress and eventually tumor cells apoptosis have been explored based on availability of chemotherapy agents that inhibit ROS-scavenging systems. These contradictory assertions suggest that antioxidant supplementation during chemotherapy treatment can have varied outcomes depending on the tumor cellular context. Therefore, understanding the antioxidant-driven molecular pathways might be crucial to design new therapeutic strategies to fight cancer progression.


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