Caspases: A Potential Therapeutic Targets in the Treatment of Alzheimer’s Disease

Jana, Kuladip

doi:10.4172/2161-1025.s2-006

Cited by 4 publications

(10 citation statements)

References 46 publications

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“…Our data suggest a role for caspase-3 in depletion of STIM1, thus linking the activated protease to loss of salivary gland function after irradiation rather than apoptosis. Consistent with this notion, caspase-3 can target and cleave various proteins not involved in apoptosis and thus contribute to regulation of critical cellular functions such as proliferation and differentiation (32)(33)(34)(35). The mechanism that determines whether caspase-3 activation triggers apoptosis has not yet been established.…”

Section: Discussionmentioning

confidence: 97%

Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway

et al. 2017

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Store-operated Ca2+ entry (SOCE) is critical for salivary gland fluid secretion. We report that radiation treatment caused persistent salivary gland dysfunction by activating a TRPM2-dependent mitochondrial pathway, leading to caspase-3–mediated cleavage of stromal interaction molecule 1 (STIM1) and loss of SOCE. After irradiation, acinar cells from the submandibular glands of TRPM2+/+, but not those from TRPM2−/− mice, displayed an increase in the concentrations of mitochondrial Ca2+ and reactive oxygen species, a decrease in mitochondrial membrane potential, and activation of caspase-3, which was associated with a sustained decrease in STIM1 abundance and attenuation of SOCE. In a salivary gland cell line, silencing the mitochondrial Ca2+ uniporter or caspase-3 or treatment with inhibitors of TRPM2 or caspase-3 prevented irradiation-induced loss of STIM1 and SOCE. Expression of exogenous STIM1 in the salivary glands of irradiated mice increased SOCE and fluid secretion. We suggest that targeting the mechanisms underlying the loss of STIM1 would be a potentially useful approach for preserving salivary gland function after radiation therapy.

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Section: Discussionmentioning

confidence: 97%

Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway

et al. 2017

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“…Alzheimer's disease is the most common neurodegenerative disorder, characterized by disturbances in short-term memory and subsequent dementia. 61 Although the exact molecular mechanisms of neuronal death is unclear, it seems that apoptosis is a major cause of AD-related neuronal death. Based upon the pertinent investigations, the amyloid beta (Aβ) has an important role in the induction of apoptosis and the pathogenesis of AD.…”

Section: Alzheimer's Diseasementioning

confidence: 99%

Caspase‐3: Structure, function, and biotechnological aspects

Asadi

Taghizadeh

Kaviani

et al. 2021

Biotech and App Biochem

211

109

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Caspase‐3, a cysteine‐aspartic acid protease, has recently attracted much attention because of its incredible roles in tissue differentiation, regeneration, and neural development. This enzyme is a key zymogen in cell apoptosis and is not activated until it is cleaved by initiator caspases during apoptotic flux. Since caspase‐3 has represented valuable capabilities in the field of medical research, biotechnological aspects of this enzyme, including the production of recombinant type, protein engineering, and designing delivery systems, have been considered as emerging therapeutic strategies in treating the apoptosis‐related disorders. To date, several advances have been made in the therapeutic use of caspase‐3 in the management of some diseases such as cancers, heart failure, and neurodegenerative disorders. In the current review, we intend to discuss the caspase‐3's structure, functions, therapeutic applications, as well as its molecular cloning, protein engineering, and relevant delivery systems.

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“…Members of the caspase family play a critical role in AD- induced neuronal apoptosis ( 39 ). Therefore, their role in AD pathology has been widely examined ( 40 , 39 , 38 , 37 , 12 , 41 ).…”

Section: Caspases In Alzheimer Diseasementioning

confidence: 99%

“…Caspases -1, -2, -3,–5, -6, -7, -8 and -9 have all been detected to be transcriptionally elevated in AD ( 41 ). Caspases may be playing a proximal role in the disease mechanisms underlying AD including promoting Aβ formation as well as linking plaques to neurofibrillary tangles ( 40 ).…”

Section: Caspases In Alzheimer Diseasementioning

confidence: 99%

The Role of Cysteine Protease in Alzheimer Disease

et al. 2016

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Introduction:Cysteine protease are biological catalysts which play a pivotal role in numerous biological reactions in organism. Much of the literature is inscribed to their biochemical significance, distribution and mechanism of action. Many diseases, e.g. Alzheimer’s disease, develop due to enzyme balance disruption. Understanding of cysteine protease’s disbalance is therefor a key to unravel the new possibilities of treatment. Cysteine protease are one of the most important enzymes for protein disruption during programmed cell death. Whether protein disruption is part of cell deaths is not enough clear in any cases. Thereafter, any tissue disruption, including proteolysis, generate more or less inflammation appearance.Review:This review briefly summarizes the current knowledge about pathological mechanism’s that results in AD, with significant reference to the role of cysteine protease in it. Based on the summary, new pharmacological approach and development of novel potent drugs with selective toxicity targeting cysteine protease will be a major challenge in years to come.

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Caspases: A Potential Therapeutic Targets in the Treatment of Alzheimer’s Disease

Cited by 4 publications

References 46 publications

Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway

Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway

Caspase‐3: Structure, function, and biotechnological aspects

The Role of Cysteine Protease in Alzheimer Disease

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