scholarly journals Accelerated pre-senile systemic amyloidosis in PACAP knockout mice - a protective role of PACAP in age-related degenerative processes

2018 ◽  
Vol 245 (4) ◽  
pp. 478-490 ◽  
Author(s):  
Dora Reglodi ◽  
Adel Jungling ◽  
Rémi Longuespée ◽  
Joerg Kriegsmann ◽  
Rita Casadonte ◽  
...  
2021 ◽  
Vol 22 (3) ◽  
pp. 1200
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama

Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.


2021 ◽  
pp. 101543
Author(s):  
Alyson L. Sujkowski ◽  
Luke Hong ◽  
R.J. Wessells ◽  
Sokol V. Todi
Keyword(s):  

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183565 ◽  
Author(s):  
Sara Kenawy ◽  
Rehab Hegazy ◽  
Azza Hassan ◽  
Siham El-Shenawy ◽  
Nawal Gomaa ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Wenzhou Huang ◽  
Peng Ao ◽  
Jian Li ◽  
Tianlong Wu ◽  
Libiao Xu ◽  
...  

Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13.


Perception ◽  
1997 ◽  
Vol 26 (1_suppl) ◽  
pp. 166-166
Author(s):  
B R Hammond ◽  
J E Náñez

Epidemiological data have identified a number of factors that influence risk of developing age-related cataract (ARC). For instance, factors that promote (eg smoking and light exposure) and factors that protect (eg antioxidants) against oxidative stress to the crystalline lens appear to increase and decrease risk of ARC, respectively. Although biochemical studies consistently support a protective role for antioxidants, the epidemiological data are inconsistent. Since ARC is a condition with a protracted latency period, it is possible that the inconsistencies present in the epidemiological literature may be due to the focus on cataractous patients. We focused on the lens health of individuals prior to cataract. Lens health was determined by measuring the optical density (OD) of the lens with a psychophysical technique. OD characterises many of the biochemical changes of the lens and is part of many systems used to classify ARC. Variance in lens OD, stratified by age, was examined for its relationship to variables thought to be important to the etiology of ARC. We report results for the relationship of lens OD to the antioxidants lutein and zeaxanthin (L and Z). For older individuals (>48 years) we noted a significant inverse relationship between dietary intake of L and Z and lens OD ( n=39, r=−0.34, p<0.015). This was not the case for younger individuals (24 – 36 years). This relationship is increased when L and Z are measured directly in the retina is a psychophysical technique. For older individuals, retinal L and Z (ie macular pigment) are inversely related to lens OD ( n=51, r=-0.47, p<0.001). These data are consistent with a role of L and Z in protecting against age-related increases in the OD of the crystalline lens.


2000 ◽  
Vol 80 (5) ◽  
pp. 759-767 ◽  
Author(s):  
Hiroyuki Yamada ◽  
Satoru Mizumo ◽  
Reiko Horai ◽  
Yoichiro Iwakura ◽  
Isamu Sugawara

2010 ◽  
Vol 04 (01) ◽  
pp. 74 ◽  
Author(s):  
Samanta Maci ◽  

Lutein and zeaxanthin are oxycarotenoids that are naturally present in the typical human diet. They are the only two dietary carotenoids selectively deposited in the macula lutea, where they are referred to as the macular pigment (MP), and in the eye lens. The rationale for the protective role of lutein in the eye stems from its ability to filter short wavelengths of visible blue light, function as an antioxidant and stabilise membrane integrity. These functions are believed to play an important role in reducing light-induced oxidative damage caused by reactive oxygen intermediates and involved in the pathogenesis of age-related degenerative disease such as age-related macular degeneration and cataract. Recent research is now paying particular attention to the blue-light-filtering properties of lutein and zeaxanthin and to the role of MP in improving visual performance.


2000 ◽  
Vol 72 (6) ◽  
pp. 1023-1026 ◽  
Author(s):  
Curtis D. Klaassen ◽  
Supratim Choudhuri

Acute Cd exposure produces liver injury, whereas chronic Cd exposure damages the kidney but not the liver. Previous experiments suggest that the low-molecular-weight, metal-binding protein metallothionein (MT) in liver protects against liver injury, but is responsible for the kidney injury observed after chronic Cd exposure. Thus, prior to the development of MT-transgenic and MT-knockout mice models, MT's role was always assumed to be a toxicological paradox, hepatoprotection but nephrotoxicity. The development of MT-transgenic and MT-knockout mice models has reconfirmed MT's protective role against Cd-induced hepatotoxicity, but it has challenged MT's suggested role in Cd-induced nephrotoxicity. In this communication, recent data using these genetically altered mice models indicate that MT protects against not only the Cd-induced hepatotoxicity, but also nephrotoxicity, hematotoxicity, immunotoxicity, and bone damage.


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