scholarly journals Lactoferrin promotes the autophagy activity during osteoblast formation via BCL2-Beclin1 signaling

2021 ◽  
Author(s):  
Dianshan Ke ◽  
Xinwen Wang ◽  
Yinquan Lin ◽  
Shengwang Wei
Keyword(s):  
Autophagy Activity

Autophagy and ageing: implications for age-related neurodegenerative diseases

2013 ◽  
Vol 55 ◽  
pp. 119-131 ◽  
Author(s):  
Bernadette Carroll ◽  
Graeme Hewitt ◽  
Viktor I. Korolchuk
Keyword(s):  
Neurodegenerative Diseases ◽  
Energy Availability ◽  
Future Studies ◽  
Intracellular Degradation ◽  
Age Related ◽  
Autophagy Induction ◽  
Social Importance ◽  
Cellular Dysfunction ◽  
Autophagy Activity ◽  
Intense Research

Autophagy is a process of lysosome-dependent intracellular degradation that participates in the liberation of resources including amino acids and energy to maintain homoeostasis. Autophagy is particularly important in stress conditions such as nutrient starvation and any perturbation in the ability of the cell to activate or regulate autophagy can lead to cellular dysfunction and disease. An area of intense research interest is the role and indeed the fate of autophagy during cellular and organismal ageing. Age-related disorders are associated with increased cellular stress and assault including DNA damage, reduced energy availability, protein aggregation and accumulation of damaged organelles. A reduction in autophagy activity has been observed in a number of ageing models and its up-regulation via pharmacological and genetic methods can alleviate age-related pathologies. In particular, autophagy induction can enhance clearance of toxic intracellular waste associated with neurodegenerative diseases and has been comprehensively demonstrated to improve lifespan in yeast, worms, flies, rodents and primates. The situation, however, has been complicated by the identification that autophagy up-regulation can also occur during ageing. Indeed, in certain situations, reduced autophagosome induction may actually provide benefits to ageing cells. Future studies will undoubtedly improve our understanding of exactly how the multiple signals that are integrated to control appropriate autophagy activity change during ageing, what affect this has on autophagy and to what extent autophagy contributes to age-associated pathologies. Identification of mechanisms that influence a healthy lifespan is of economic, medical and social importance in our ‘ageing’ world.

scholarly journals Autophagy activity is associated with membranous sodium iodide symporter expression and clinical response to radioiodine therapy in non-medullary thyroid cancer

Autophagy ◽  
2016 ◽  
Vol 12 (7) ◽  
pp. 1195-1205 ◽  
Author(s):  
Theo S. Plantinga ◽  
Marika H. Tesselaar ◽  
Hans Morreau ◽  
Eleonora P. M. Corssmit ◽  
Brigith K. Willemsen ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Clinical Response ◽  
Sodium Iodide ◽  
Medullary Thyroid Cancer ◽  
Radioiodine Therapy ◽  
Sodium Iodide Symporter ◽  
Medullary Thyroid ◽  
Autophagy Activity

scholarly journals Effects of AANAT overexpression on the inflammatory responses and autophagy activity in the cellular and transgenic animal levels

Autophagy ◽  
2018 ◽  
Vol 14 (11) ◽  
pp. 1850-1869 ◽  
Author(s):  
Jingli Tao ◽  
Minghui Yang ◽  
Hao Wu ◽  
Teng Ma ◽  
Changjiu He ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Transgenic Animal ◽  
Autophagy Activity

Autophagy Markers p62, LC3II and Beclin1 Correlate with Clark Levels in Melanoma Tumors

2021 ◽  
Author(s):  
Reyhaneh Hizomi Arani ◽  
Hadiseh Mohammadpour ◽  
Mohammad Amin Moosavi ◽  
Alireza Abdollahi ◽  
Marveh Rahmati
Keyword(s):  
Gene Expression ◽  
Tumor Progression ◽  
Early Stage ◽  
Mitotic Rate ◽  
Beclin 1 ◽  
Roc Curve Analysis ◽  
Mechanism Of Degradation ◽  
Associated Proteins ◽  
Potential Prognostic Factor ◽  
Autophagy Activity

Abstract BackgroundThe prognosis of melanoma depends on early diagnosis and timely treatment. Autophagy as a mechanism of degradation/recycling of cellular debris, has potential to be evaluated as prognostic biomarker in current research. MethodsIn this study, ATG5 and Beclin 1 gene expression in different Clark levels of melanoma were evaluated in a retrospective study of 10 years in the cancer institute of Tehran, Iran. The autophagy activity and the correlation with clinicopathological data were also investigated in a tissue microarray series of 52 melanomas after immunohistochemical staining for the autophagy-associated proteins p62, LC3II and Beclin1. The possibility of autophagy biomarkers were assessed by ROC curve analysis.ResultsThe patterns of ATG5 and Beclin1 gene expression are different. While ATG5 was increased in the early stage and then decreased as the stage was progressed in comparison to tumor margin, the Beclin1 expression was decreased and not altered during tumor progression. However, Beclin1 expression at the protein level was increased with tumor progression. The expression of LC3II was also raised while the p62 levels were declined as the tumor progressed, suggesting an increased autophagy activity in melanoma patients. Melanoma ulceration was positively correlated with Beclin 1 and LC3II expression and inversely correlated with p62 (p<0.05). Autophagy markers expression did not significantly correlate with melanoma mitotic rate and thickness. ConclusionsAutophagy is a potential prognostic factor in the early stage of melanoma and could be considered as a therapeutic target.

Rutin protects Huntington's disease through the insulin/IGF1 (IIS) signaling pathway and autophagy activity: Study in Caenorhabditis elegans model

2020 ◽  
Vol 141 ◽  
pp. 111323 ◽  
Author(s):  
Larissa Marafiga Cordeiro ◽  
Marina Lopes Machado ◽  
Aline Franzen da Silva ◽  
Fabiane Bicca Obetine Baptista ◽  
Tássia Limana da Silveira ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Signaling Pathway ◽  
Autophagy Activity

scholarly journals Role of Nutrient-Sensing Signals in the Pathogenesis of Diabetic Nephropathy

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Shinji Kume ◽  
Daisuke Koya ◽  
Takashi Uzu ◽  
Hiroshi Maegawa
Keyword(s):  
Diabetic Nephropathy ◽  
Therapeutic Potential ◽  
Nutrient Sensing ◽  
Tubular Cells ◽  
New Findings ◽  
Proximal Tubular ◽  
Stage Renal Disease ◽  
End Stage ◽  
Autophagy Activity

Diabetic nephropathy is the leading cause of end-stage renal disease worldwide. The multipronged drug approach still fails to fully prevent the onset and progression of diabetic nephropathy. Therefore, a new therapeutic target to improve the prognosis of diabetic nephropathy is urgently required. Nutrient-sensing signals and their related intracellular machinery have evolved to combat prolonged periods of starvation in mammals; and these systems are conserved in the kidney. Recent studies have suggested that the activity of three nutrient-sensing signals, mTORC1, AMPK, and Sirt1, is altered in the diabetic kidney. Furthermore, autophagy activity, which is regulated by the above-mentioned nutrient-sensing signals, is also altered in both podocytes and proximal tubular cells under diabetic conditions. Under diabetic conditions, an altered nutritional state owing to nutrient excess may disturb cellular homeostasis regulated by nutrient-responsible systems, leading to exacerbation of organelle dysfunction and diabetic nephropathy. In this review, we discuss new findings showing relationships between nutrient-sensing signals, autophagy, and diabetic nephropathy and suggest the therapeutic potential of nutrient-sensing signals in diabetic nephropathy.

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