The Charnoly body : a novel biomarker of mitochondrial bioenergetics /
Diversified physicochemical injuries trigger Charnoly body (CB) formation as pleomorphic, electron-dense, multi-lamellar stacks of nonfunctional mitochondrial membranes in the most vulnerable cell. Free radicals induce downregulation of mitochondrial DNA, microRNA, AgNOR, and epigenetics to trigger...
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Main Author: | |
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Format: | Electronic eBook |
Language: | English |
Published: |
Boca Raton, FL :
CRC Press, Taylor & Francis Group,
2019.
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Online Access: |
OCLC metadata license agreement Full text (WIT users only) |
Summary: | Diversified physicochemical injuries trigger Charnoly body (CB) formation as pleomorphic, electron-dense, multi-lamellar stacks of nonfunctional mitochondrial membranes in the most vulnerable cell. Free radicals induce downregulation of mitochondrial DNA, microRNA, AgNOR, and epigenetics to trigger CB molecular pathogenesis. CB is eliminated by energy (ATP)-driven lysosome-dependent charnolophagy as a basic molecular mechanism of intracellular detoxification to prevent acute and chronic diseases. Accumulation of CB at the junction of axon hillock and charnolosome (CS) at the synapses causes cognitive impairments; whereas, nonspecific induction of CB causes GIT stress, myelosuppression, alopecia, neurotoxicity, cardiotoxicity, and infertility in multidrug-resistant malignancies. Hence, stem cell-specific CB, charnolophagy, and CS agonists/antagonists are introduced as novelcharnolopharmacotherapeutics for the successful treatment of cardiovascular diseases, neurodegenerative diseases, infectious diseases, drug addiction, and cancer. Nanoparticles to improve drug delivery, CS exocytosis, and disease-specific spatiotemporal charnolosomics employing correlative and combinatorial bioinformatics boost mitochondrial bioenergetics through balanced diet, exercise, and antioxidants. The book will be of interest to medical scientists and practitioners. |
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Item Description: | "A Science Publishers book." |
Physical Description: | 1 online resource. |
ISBN: | 9781315150710 1315150719 9781351366717 1351366718 9781351366700 135136670X 9781351366694 1351366696 |
Source of Description, Etc. Note: | OCLC-licensed vendor bibliographic record. |