Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases
Alzheimer’s disease, type 2 diabetes, and non-alcoholic steatohepatitis (NASH) constitute increasingly prevalent disorders. Individuals with type 2 diabetes are well-known to be susceptible to Alzheimer’s disease. Although the pathogenesis of each disorder is multifactorial and the causal relation r...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-02-01
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| Series: | Frontiers in Molecular Biosciences |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fmolb.2022.1063632/full |
| _version_ | 1811173116892676096 |
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| author | Tetsumori Yamashima Tetsumori Yamashima Takuya Seike Shinji Oikawa Hatasu Kobayashi Hidenori Kido Masahiro Yanagi Daisuke Yamamiya Shihui Li Piyakarn Boontem Eishiro Mizukoshi |
| author_facet | Tetsumori Yamashima Tetsumori Yamashima Takuya Seike Shinji Oikawa Hatasu Kobayashi Hidenori Kido Masahiro Yanagi Daisuke Yamamiya Shihui Li Piyakarn Boontem Eishiro Mizukoshi |
| author_sort | Tetsumori Yamashima |
| collection | DOAJ |
| description | Alzheimer’s disease, type 2 diabetes, and non-alcoholic steatohepatitis (NASH) constitute increasingly prevalent disorders. Individuals with type 2 diabetes are well-known to be susceptible to Alzheimer’s disease. Although the pathogenesis of each disorder is multifactorial and the causal relation remains poorly understood, reactive oxygen species (ROS)-induced lipid and protein oxidation conceivably plays a common role. Lipid peroxidation product was recently reported to be a key factor also for non-alcoholic steatohepatitis, because of inducing hepatocyte degeneration/death. Here, we focus on implication of the representative lipid-peroxidation product ‘hydroxynonenal’ for the cell degeneration/death of brain, pancreas, and liver. Since Hsp70.1 has dual roles as a chaperone and lysosomal membrane stabilizer, hydroxynonenal-mediated oxidative injury (carbonylation) of Hsp70.1 was highlighted. After intake of high-fat diets, oxidation of free fatty acids in mitochondria generates ROS which enhance oxidation of ω-6 polyunsaturated fatty acids (PUFA) involved within biomembranes and generate hydroxynonenal. In addition, hydroxynonenal is generated during cooking deep-fried foods with vegetable oils especially containing linoleic acids. These intrinsic and exogenous hydroxynonenal synergically causes an increase in its serum and organ levels to induce Hsp70.1 oxidation. As it is amphiphilic; being water-soluble but displays strong lipophilic characteristics, hydroxynonenal can diffuse within the cells and react with targets like senile and/or atheromatous plaques outside the cells. Hydroxynonenal can deepen and expand lysosomal injuries by facilitating ‘calpain-mediated cleavage of the carbonylated Hsp70.1’. Despite the unique anatomical, physiological, and biochemical characteristics of each organ for its specific disease, there should be a common cascade of the cell degeneration/death which is caused by hydroxynonenal. This review aims to implicate hydroxynonenal-mediated Hsp70.1 carbonylation for lysosomal membrane permeabilization/rupture and the resultant cathepsin leakage for inducing cell degeneration/death. Given the tremendous number of worldwide people suffering various lifestyle-related diseases, it is valuable to consider how ω-6 PUFA-rich vegetable oils is implicated for the organ disorder. |
| first_indexed | 2024-04-10T17:42:34Z |
| format | Article |
| id | doaj.art-cc785862cf064f9fb7b307fb88fadf26 |
| institution | Directory Open Access Journal |
| issn | 2296-889X |
| language | English |
| last_indexed | 2024-04-10T17:42:34Z |
| publishDate | 2023-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Biosciences |
| spelling | doaj.art-cc785862cf064f9fb7b307fb88fadf262023-02-03T12:12:59ZengFrontiers Media S.A.Frontiers in Molecular Biosciences2296-889X2023-02-01910.3389/fmolb.2022.10636321063632Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseasesTetsumori Yamashima0Tetsumori Yamashima1Takuya Seike2Shinji Oikawa3Hatasu Kobayashi4Hidenori Kido5Masahiro Yanagi6Daisuke Yamamiya7Shihui Li8Piyakarn Boontem9Eishiro Mizukoshi10Department of Psychiatry and Behavioral Science, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Cell Metabolism and Nutrition, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Tsu, JapanDepartment of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Tsu, JapanDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Cell Metabolism and Nutrition, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, JapanAlzheimer’s disease, type 2 diabetes, and non-alcoholic steatohepatitis (NASH) constitute increasingly prevalent disorders. Individuals with type 2 diabetes are well-known to be susceptible to Alzheimer’s disease. Although the pathogenesis of each disorder is multifactorial and the causal relation remains poorly understood, reactive oxygen species (ROS)-induced lipid and protein oxidation conceivably plays a common role. Lipid peroxidation product was recently reported to be a key factor also for non-alcoholic steatohepatitis, because of inducing hepatocyte degeneration/death. Here, we focus on implication of the representative lipid-peroxidation product ‘hydroxynonenal’ for the cell degeneration/death of brain, pancreas, and liver. Since Hsp70.1 has dual roles as a chaperone and lysosomal membrane stabilizer, hydroxynonenal-mediated oxidative injury (carbonylation) of Hsp70.1 was highlighted. After intake of high-fat diets, oxidation of free fatty acids in mitochondria generates ROS which enhance oxidation of ω-6 polyunsaturated fatty acids (PUFA) involved within biomembranes and generate hydroxynonenal. In addition, hydroxynonenal is generated during cooking deep-fried foods with vegetable oils especially containing linoleic acids. These intrinsic and exogenous hydroxynonenal synergically causes an increase in its serum and organ levels to induce Hsp70.1 oxidation. As it is amphiphilic; being water-soluble but displays strong lipophilic characteristics, hydroxynonenal can diffuse within the cells and react with targets like senile and/or atheromatous plaques outside the cells. Hydroxynonenal can deepen and expand lysosomal injuries by facilitating ‘calpain-mediated cleavage of the carbonylated Hsp70.1’. Despite the unique anatomical, physiological, and biochemical characteristics of each organ for its specific disease, there should be a common cascade of the cell degeneration/death which is caused by hydroxynonenal. This review aims to implicate hydroxynonenal-mediated Hsp70.1 carbonylation for lysosomal membrane permeabilization/rupture and the resultant cathepsin leakage for inducing cell degeneration/death. Given the tremendous number of worldwide people suffering various lifestyle-related diseases, it is valuable to consider how ω-6 PUFA-rich vegetable oils is implicated for the organ disorder.https://www.frontiersin.org/articles/10.3389/fmolb.2022.1063632/fullAlzheimer’s diseasecalpain-cathepsin hypothesishydroxynonenalnon-alcoholic steatohepatitistype 2 diabetes |
| spellingShingle | Tetsumori Yamashima Tetsumori Yamashima Takuya Seike Shinji Oikawa Hatasu Kobayashi Hidenori Kido Masahiro Yanagi Daisuke Yamamiya Shihui Li Piyakarn Boontem Eishiro Mizukoshi Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases Frontiers in Molecular Biosciences Alzheimer’s disease calpain-cathepsin hypothesis hydroxynonenal non-alcoholic steatohepatitis type 2 diabetes |
| title | Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases |
| title_full | Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases |
| title_fullStr | Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases |
| title_full_unstemmed | Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases |
| title_short | Hsp70.1 carbonylation induces lysosomal cell death for lifestyle-related diseases |
| title_sort | hsp70 1 carbonylation induces lysosomal cell death for lifestyle related diseases |
| topic | Alzheimer’s disease calpain-cathepsin hypothesis hydroxynonenal non-alcoholic steatohepatitis type 2 diabetes |
| url | https://www.frontiersin.org/articles/10.3389/fmolb.2022.1063632/full |
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