scholarly journals Repertoires of Autophagy in the Pathogenesis of Ocular Diseases

2015 ◽  
Vol 35 (5) ◽  
pp. 1663-1676 ◽  
Author(s):  
Yu-jie Li ◽  
Qin Jiang ◽  
Guo-fan Cao ◽  
Jin Yao ◽  
Biao Yan
Keyword(s):  
Infectious Diseases ◽  
Neurodegenerative Diseases ◽  
Therapeutic Target ◽  
Human Diseases ◽  
Pathological Feature ◽  
Ocular Diseases ◽  
Pharmacological Manipulation ◽  
Cytoplasmic Proteins ◽  
Related Proteins

Autophagy is an important intracellular degradative process that delivers cytoplasmic proteins to lysosome for degradation. Dysfunction of autophagy is implicated in several human diseases, such as neurodegenerative diseases, infectious diseases, and cancers. Autophagy-related proteins are constitutively expressed in the eye. Increasing studies have revealed that abnormal autophagy is an important pathological feature of several ocular diseases. Pharmacological manipulation of autophagy may provide an alternative therapeutic target for some ocular diseases. In this manuscript, we reviewed the relevant progress about the role of autophagy in the pathogenesis of ocular diseases.

scholarly journals Does Irisin Link Physical Exercise with Alzheimer’s Disease?

2018 ◽  
Author(s):  
Dewan Md. Sumsuzzman ◽  
Yunho Jin ◽  
Jeonghyun Choi ◽  
Sang-Rae Lee ◽  
Yonggeun Hong
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Neurodegenerative Diseases ◽  
Telomere Length ◽  
Neurotrophic Factors ◽  
Therapeutic Target ◽  
Potential Role ◽  
Human Diseases ◽  
Nervous Systems ◽  
Beneficial Effects

Irisin, a skeletal muscle-secreted myokine, produced in response to physical exercise, has protective functions in both the central and the peripheral nervous systems, including the regulation of brain-derived neurotrophic factors and modification of telomere length. Such beneficial effects may inhibit or delay the emergence of neurodegenerative diseases, including Alzheimer’s disease (AD). This review is based on the hypothesis that irisin produced by physical exercise helps control AD progression. Herein, we describe the physiology of irisin and its potential role in delaying or preventing AD. Although current and ongoing studies on irisin show promising results, further research is required to clarify its potential as a meaningful therapeutic target for treating human diseases.

scholarly journals Chemistry-Assisted Proteomic Profiling of O-GlcNAcylation

2021 ◽  
Vol 9 ◽  
Author(s):  
Qiang Zhu ◽  
Wen Yi
Keyword(s):  
Mass Spectrometry ◽  
Neurodegenerative Diseases ◽  
Normal Cell ◽  
Functional Role ◽  
Human Diseases ◽  
Cell Physiology ◽  
Proteomic Profiling ◽  
Detection Technologies

The modification on proteins with O-linked N-acetyl-β-D-glucosamine (O-GlcNAcylation) is essential for normal cell physiology. Dysregulation of O-GlcNAcylation leads to many human diseases, such as cancer, diabetes and neurodegenerative diseases. Recently, the functional role of O-GlcNAcylation in different physiological states has been elucidated due to the booming detection technologies. Chemical approaches for the enrichment of O-GlcNAcylated proteins combined with mass spectrometry-based proteomics enable the profiling of protein O-GlcNAcylation in a system-wide level. In this review, we summarize recent progresses on the enrichment and proteomic profiling of protein O-GlcNAcylation.

scholarly journals Suppressor T Cells in Human Diseases

2004 ◽  
Vol 200 (3) ◽  
pp. 273-276 ◽  
Author(s):  
Clare Baecher-Allan ◽  
David A. Hafler
Keyword(s):  
T Cells ◽  
Infectious Diseases ◽  
Immune Responses ◽  
Autoimmune Diseases ◽  
Peripheral Tolerance ◽  
Human Diseases ◽  
Suppressor T Cells ◽  
Wide Range ◽  
Human Immune

Although central and peripheral tolerance are important for the regulation of human immune responses to self- and microbial antigens, an important role of suppressor CD4+ CD25+ T cells is suggested from the recent investigations of human autoimmune diseases and HIV. These new data provide increasing evidence that altered function of CD4+ CD25+ T cells may be an important factor in a wide range of human inflammatory and infectious diseases.

scholarly journals UNC-45A Weakens and Breaks MT Lattice Independent of its Effect on Non-Muscle Myosin II

2020 ◽  
Author(s):  
Juri Habicht ◽  
Ashley Mooneyham ◽  
Asumi Hoshino ◽  
Mihir Shetty ◽  
Xiaonan Zhang ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Myosin Ii ◽  
Human Diseases ◽  
Therapeutic Implications ◽  
Associated Functions ◽  
Muscle Myosin ◽  
First Time ◽  
In Cells

AbstractIn invertebrates, UNC-45 regulates myosin stability and functions. Vertebrates have two distinct isoforms of the protein: UNC-45B, expressed in muscle cells only and UNC-45A, expressed in all cells and implicated in regulating both Non-Muscle Myosin II (NMII)- and microtubule (MT)-associated functions. Here we show for the first time that: a) in vitro UNC-45A binds to the MT lattice and weakens its integrity leading to MT bending, breakage and depolymerization, b) in cells, UNC-45A overexpression causes loss of MT mass and increase in MT breakages, c) both in vitro and in cells, UNC-45A destabilizes MTs independent of its NMII C-terminal binding domain and destabilization occurs even in presence of the NMII inhibitor blebbistatin. These findings are consistent with a not mutually exclusive but rather dual role of UNC-45A in regulating NMII activity and MT stability.Because many human diseases, from cancer to neurodegenerative diseases, are caused by or associated with deregulation of MT stability our findings have profound implications in both, the biology of MTs as well as the biology of human diseases and possible therapeutic implications for their treatment.

scholarly journals Small RNAs, Big Diseases

2020 ◽  
Vol 21 (16) ◽  
pp. 5699 ◽  
Author(s):  
Iwona Rzeszutek ◽  
Aditi Singh
Keyword(s):  
Neurodegenerative Diseases ◽  
Small Rnas ◽  
Review Article ◽  
Human Diseases ◽  
Therapeutic Approaches ◽  
Related Research ◽  
The Past ◽  
Different Types

The past two decades have seen extensive research done to pinpoint the role of microRNAs (miRNAs) that have led to discovering thousands of miRNAs in humans. It is not, therefore, surprising to see many of them implicated in a number of common as well as rare human diseases. In this review article, we summarize the progress in our understanding of miRNA-related research in conjunction with different types of cancers and neurodegenerative diseases, as well as their potential in generating more reliable diagnostic and therapeutic approaches.

scholarly journals The Interplay between Ca2+ Signaling Pathways and Neurodegeneration

2019 ◽  
Vol 20 (23) ◽  
pp. 6004 ◽  
Author(s):  
Ureshino ◽  
Erustes ◽  
Bassani ◽  
Wachilewski ◽  
Guarache ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Temporal Organization ◽  
Amyloid Peptide ◽  
Physiological Processes ◽  
Stress Energy ◽  
The Central Nervous System ◽  
Β Amyloid Peptide ◽  
And Function ◽  
Related Proteins

Calcium (Ca2+) homeostasis is essential for cell maintenance since this ion participates in many physiological processes. For example, the spatial and temporal organization of Ca2+ signaling in the central nervous system is fundamental for neurotransmission, where local changes in cytosolic Ca2+ concentration are needed to transmit information from neuron to neuron, between neurons and glia, and even regulating local blood flow according to the required activity. However, under pathological conditions, Ca2+ homeostasis is altered, with increased cytoplasmic Ca2+ concentrations leading to the activation of proteases, lipases, and nucleases. This review aimed to highlight the role of Ca2+ signaling in neurodegenerative disease-related apoptosis, where the regulation of intracellular Ca2+ homeostasis depends on coordinated interactions between the endoplasmic reticulum, mitochondria, and lysosomes, as well as specific transport mechanisms. In neurodegenerative diseases, alterations-increased oxidative stress, energy metabolism alterations, and protein aggregation have been identified. The aggregation of α-synuclein, β-amyloid peptide (Aβ), and huntingtin all adversely affect Ca2+ homeostasis. Due to the mounting evidence for the relevance of Ca2+ signaling in neuroprotection, we would focus on the expression and function of Ca2+ signaling-related proteins, in terms of the effects on autophagy regulation and the onset and progression of neurodegenerative diseases.

scholarly journals The Role of Tau in Neurodegenerative Diseases and Its Potential as a Therapeutic Target

Scientifica ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-20 ◽  
Author(s):  
Michael S. Wolfe
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurological Disorders ◽  
Pathological Feature ◽  
Tau Pathology ◽  
Gene Encoding ◽  
Protein Tau ◽  
Molecular Events ◽  
Potential Therapeutics ◽  
Key Questions

The abnormal deposition of proteins in and around neurons is a common pathological feature of many neurodegenerative diseases. Among these pathological proteins, the microtubule-associated protein tau forms intraneuronal filaments in a spectrum of neurological disorders. The discovery that dominant mutations in theMAPTgene encoding tau are associated with familial frontotemporal dementia strongly supports abnormal tau protein as directly involved in disease pathogenesis. This and other evidence suggest that tau is a worthwhile target for the prevention or treatment of tau-associated neurodegenerative diseases, collectively called tauopathies. However, it is critical to understand the normal biological roles of tau, the specific molecular events that induce tau to become neurotoxic, the biochemical nature of pathogenic tau, the means by which pathogenic tau exerts neurotoxicity, and how tau pathology propagates. Based on known differences between normal and abnormal tau, a number of approaches have been taken toward the discovery of potential therapeutics. Key questions still remain open, such as the nature of the connection between the amyloid-βprotein of Alzheimer’s disease and tau pathology. Answers to these questions should help better understand the nature of tauopathies and may also reveal new therapeutic targets and strategies.

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