ABSTRACT
BACKGROUND: Neurological disorders have been continuously contributing to the global disease burden and affect millions of people worldwide. Researchers strive hard to extract out the ultimate cure and serve for the betterment of the society, and yet the treatments available provide only symptomatic relief. Aging and abnormal mutations seem to be the major culprits responsible for neurotoxicity and neuronal death. One of the major causes of these neurological disorders that has been paid utmost attention recently, is Autophagic Dysfunction. AIM: The aim of the study was to understand the autophagic process, its impairment in neurological disorders and targeting the impairments as a therapeutic option for the said disorders. METHODS: For the purpose of review, we carried out an extensive literature study to excerpt the series of steps involved in autophagy and to understand the mechanism of autophagic impairment occurring in a range of neurodegenerative and neuropsychiatric disorders like Parkinson, Alzheimer, Depression, Schizophrenia, Autism etc. The review also involved the exploration of certain molecules that can help in triggering the compromised autophagic members. RESULTS: We found that, a number of genes, proteins, receptors and transcription factors interplay to bring about autophagy and plethora of neurological disorders are associated with the diminished expression of one or more autophagic member leading to inhibition of autophagy. CONCLUSION: Autophagy is a significant process for the removal of misfolded, abnormal, damaged protein aggregates and nonfunctional cell organelles in order to suppress neurodegeneration. Therefore, triggering autophagy could serve as an important therapeutic target to treat neurological disorders.
Subject(s)
Neurodegenerative Diseases , Aging , Autophagy , Carrier Proteins , Humans , Neurodegenerative Diseases/metabolism , Proteins/metabolismABSTRACT
The significance of mesenchymal stem cells (MSCs) for tissue repair and regeneration is widely recognized. The pleiotropic nature of MSCs is demonstrated by their potential for proliferation and differentiation, and paracrine secretions, thereby making them ideal candidates for cell replacement therapy. Tissue resident MSCs are engaged in homeostasis under normal wear and tear. However, stem cell therapy may be applicable if damage cannot be repaired by normal homeostatic mechanisms. The safety of MSCs has been clearly established in clinical trials but their efficacy remains questionable. The efficacy of MSCs depends on several factors, such as their viability, functional status in terms of secretome secretions, and the in-vivo scenario after transplantation. The performance of MSCs is regulated by their micro-environmental conditions and cues. The so-called MSC niche comprises physical, chemical, and biological components, which play key roles in determining the fate of MSCs. MSCs scaled up for transplantation purposes comprise a disorganized mass of cells, which needs to be directed to perform the required function. Thus, MSCs need to be directed toward an expected target activity in human patients. This review focuses on the various methods that can be used to guide stem cells for cutaneous repair.
ABSTRACT
Diabetes mellitus is the 7th leading cause of death worldwide. Diabetes can affect the organ systems and lead to serious complications, majorly categorized as macrovascular complications, microvascular complications, and diabetic wounds. Foot ulcer develops in 15-25% diabetic patients. In diabetic wound, there is an impairment in growth factor, neuropeptide, matrix metalloproteinases, angiogenesis, and immune system. Many approaches are being experimented to manage this major complication of diabetic foot, but unfortunately with lower success rate. Stem cell is an upcoming field which is being explored in the world of diabetes. Hence, this review is designed to understand the basic pathogenesis and complications of types of diabetes and the role of stem cells in a diabetic wound and the benefits related to it.