scholarly journals The Role of Autophagy in Osteoarthritis

Author(s):  
Ran Duan ◽  
Hui Xie ◽  
Zheng-Zhao Liu

Chondrocytes are the only cell type in normal cartilage. The pathological changes of osteoarthritis (OA) mostly revolve around the apoptosis and dysfunction of chondrocytes. Autophagy, as an intracellular degradation system that maintains the steady state of energy metabolism in cells, has been shown to restore the function of damaged chondrocytes, alleviating the occurrence and progression of OA. In this review, we explored the relationship between autophagy and OA and the key molecules of autophagy pathway that regulate the progression of OA, providing new ideas for OA treatment by targeting autophagy.

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Pan Luo ◽  
Fuqiang Gao ◽  
Dongsheng Niu ◽  
Xichun Sun ◽  
Qiang Song ◽  
...  

Chondrocytes are the sole cellular constituents of normal cartilage. The degeneration and apoptosis of these cells are considered the main cause of osteoarthritis (OA). Previous studies have suggested that the enhancement of autophagy in chondrocytes can delay the progression of osteoarthritis by affecting intracellular metabolic activity, i.e., by regulating the metabolism of nutrients, which can delay cell aging and death. In this review, we explored the relationship between autophagy and chondrocyte metabolism and provided new ideas for the prevention and treatment of OA.


2020 ◽  
Vol 11 ◽  
Author(s):  
Ziqi Shao ◽  
Shanshan Dou ◽  
Junge Zhu ◽  
Huiqing Wang ◽  
Dandan Xu ◽  
...  

Mitochondria are important places for eukaryotes to carry out energy metabolism and participate in the processes of cell differentiation, cell information transmission, and cell apoptosis. Autophagy is a programmed intracellular degradation process. Mitophagy, as a selective autophagy, is an evolutionarily conserved cellular process to eliminate dysfunctional or redundant mitochondria, thereby fine-tuning the number of mitochondria and maintaining energy metabolism. Many stimuli could activate mitophagy to regulate related physiological processes, which could ultimately reduce or aggravate the damage caused by stimulation. Stroke is a common disease that seriously affects the health and lives of people around the world, and ischemic stroke, which is caused by cerebral vascular stenosis or obstruction, accounts for the vast majority of stroke. Abnormal mitophagy is closely related to the occurrence, development and pathological mechanism of ischemic stroke. However, the exact mechanism of mitophagy involved in ischemic stroke has not been fully elucidated. In this review, we discuss the process and signal pathways of mitophagy, the potential role of mitophagy in ischemic stroke and the possible signal transduction pathways. It will help deepen the understanding of mitophagy and provide new ideas for the treatment of ischemic stroke.


Author(s):  
L. Fituni

The author presents his own original conception of the 2011 Arab upheavals. First, he tries to find parallels between the Arab Spring and the 19th century European Spring of Peoples. Second, he dwells on the idea of three types of transition in the Arab World: economic, demographic, and ideological. Third, he reflects on the issues of democracy and autocracy in the Arab countries emphasizing the role of youth. Fourth, he puts forward some new ideas as regards the relationship between Europe and the Arab World, offering such terms as “democratic internationalism” and “young democratic safety belt” in the Mediterranean region.


1985 ◽  
Vol 249 (3) ◽  
pp. C297-C303 ◽  
Author(s):  
M. E. Bromberg ◽  
R. W. Sevy ◽  
J. L. Daniel ◽  
L. Salganicoff

The relationship between tension and myosin 20,000-Da light chain phosphorylation in intact nonmuscle cells was investigated using a preparation of thrombin-activated, irreversibly aggregated platelets known as the platelet strip. Steady-state levels of tension generated by the platelet strip were found to be linearly related to the level of myosin phosphorylation. This relationship was observed during dose-dependent relaxation induced by the adenylate cyclase activators prostaglandin (PG) E1 and PGI2, and during contraction induced by ADP, epinephrine, and the prostaglandin endoperoxide analogue U-46619, which did not appreciably alter the basal level of adenosine 3',5'-cyclic monophosphate in the preparation. The fully relaxed platelet strip, in the absence of external Ca2+, was associated with a level of 12% light chain phosphorylation, which increased to 72% on maximal contraction. During both relaxation and contraction, changes in myosin phosphorylation were also found to precede or coincide with tension changes. Furthermore, steady-state contraction induced by ADP was associated with a maintained elevation in the level of myosin phosphorylation. These results support the concept that myosin phosphorylation is an important regulatory mechanism for contractility in platelets.


2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Betty N. Wu ◽  
Anthony J. O'Sullivan

Women have a higher proportion of body fat compared to men. However, women consume fewer kilojoules per kilogram lean mass and burn fat more preferentially during exercise compared with men. During gestation, women store even greater amounts of fat that cannot be solely attributed to increased energy intake. These observations suggest that the relationship between kilojoules consumed and kilojoules utilised is different in men and women. The reason for these sex differences in energy metabolism is not known; however, it may relate to sex steroids, differences in insulin resistance, or metabolic effects of other hormones such as leptin. When considering lifestyle modifications, sex differences in energy metabolism should be considered. Moreover, elucidating the regulatory role of hormones in energy homeostasis is important for understanding the pathogenesis of obesity and perhaps in the future may lead to ways to reduce body fat with less energy restriction.


2019 ◽  
Vol 69 (6) ◽  
pp. 638-654
Author(s):  
Deaa Al-Deen Al-Sraheen ◽  
Khaldoon Ahmad Al Daoud

While often criticized, the independence of directors remains a crucial criterion for evaluating the effectiveness of the monitoring role of boards. This study examines the relationship between board independence and earnings management, paying attention to moderation role of family ownership concentration on this relationship using a sample of services companies listed on Amman Stock Exchange ASE. This study documented a significant and negative association between board independence and earnings management. In addition, the moderating role of family ownership concentration on this relationship was also negative. Thus, the board’s monitoring function was inefficient due to the concentration of ownership. These results were obtained through using multiple and sequential regression analysis for the research data from 2013 to 2016. This study provides new ideas for future research such as examining the impacts of the migration of capitals and investors from neighbouring countries such as Syria and Iraq.


2009 ◽  
Vol 11 (3) ◽  
pp. 281-295 ◽  

Astrocytes are the main neural cell type responsible for the maintenance of brain homeostasis. They form highly organized anatomical domains that are interconnected into extensive networks. These features, along with the expression of a wide array of receptors, transporters, and ion channels, ideally position them to sense and dynamically modulate neuronal activity. Astrocytes cooperate with neurons on several levels, including neurotransmitter trafficking and recycling, ion homeostasis, energy metabolism, and defense against oxidative stress. The critical dependence of neurons upon their constant support confers astrocytes with intrinsic neuroprotective properties which are discussed here. Conversely, pathogenic stimuli may disturb astrocytic function, thus compromising neuronal functionality and viability. Using neuroinflammation, Alzheimer's disease, and hepatic encephalopathy as examples, we discuss how astrocytic defense mechanisms may be overwhelmed in pathological conditions, contributing to disease progression.


Author(s):  
Anna Gannon

This is the first scholarly art-historical appraisal of Anglo-Saxon coinage, from its inception in the late sixth century to Offa's second reform of the penny c.792. Outside numismatic circles, this material has largely been ignored because of its complexity, yet artistically this is the most vibrant period of English coinage, with die-cutters showing flair and innovation and employing hundreds of different designs in their work. By analysing the iconography of the early coinage, this book intends to introduce its rich legacy to a wide audience. Anna Gannon divides the designs of the coins into four main categories: busts (including attributes and drapery), human figures, animals and geometrical patterns, presenting prototypes, sources of the repertoire and parallels with contemporary visual arts for each motif. The comparisons demonstrate the central role of coins in the eclectic visual culture of the time, with the advantages of official sanctioning and wide circulation to support and diffuse new ideas and images. The sources of the motifs clarify the relationship between the many designs of the complex Secondary phase (c.710-50). Contemporary literature and theological writings often offer the key to the interpretation of motifs, hinting at a universal preoccupation with religious themes. The richness of designs and display of learning point to a sophisticated patronage with access to exotic prototypes, excellent craftsmanship and wealth; it is likely that minsters, as rich, learned, and well-organized institutions, were behind some of the coinage. After the economic crises of the mid-eighth century this flamboyant iconography was swept away: with the notable exeption of the coins of Offa, still displaying exciting designs of high quality and inventiveness, reformed issues bore royal names and titles, and strove towards uniformity.


Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 767
Author(s):  
Carmela Rinaldi ◽  
Luigi Donato ◽  
Simona Alibrandi ◽  
Concetta Scimone ◽  
Rosalia D’Angelo ◽  
...  

The neurovascular unit (NVU) is a relatively recent concept that clearly describes the relationship between brain cells and their blood vessels. The components of the NVU, comprising different types of cells, are so interrelated and associated with each other that they are considered as a single functioning unit. For this reason, even slight disturbances in the NVU could severely affect brain homeostasis and health. In this review, we aim to describe the current state of knowledge concerning the role of oxidative stress on the neurovascular unit and the role of a single cell type in the NVU crosstalk.


2021 ◽  
Vol 15 ◽  
Author(s):  
Ya-Ting Huang ◽  
Fen-Fang Hong ◽  
Shu-Long Yang

Vascular dementia (VD), a cerebrovascular disease which causes cognitive impairment, is one of the significant factors that affects the quality of senectitude. Atherosclerosis (AS) is a chronic inflammatory syndrome and closely associated with VD. Analyzing the role of AS in VD contribute greatly to its early detection and prevention, but their relationship has not been integrated into a complete network. This review summarizes AS biomarkers as VD predictors for the first time and describes the direct mechanisms of AS causing VD from five aspects: vascular morphogenesis, hemodynamic change, neurovascular unit damage (NVU), oxidative stress, and microRNA (miRNA). Finally, it discriminates the relationship between AS and VD in common risk factors which can be disease or some molecules. In particular, these data imply that the role of AS in VD is not only a pathogenic factor but also a comorbidity in VD. This review aims to bring new ideas for the prediction and treatment of VD.


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