Targeting Mitochondrial Complex I Deficiency in MPP < sup > + < /sup > /MPTP-induced Parkinson's Disease Cell Culture and Mouse Models by Transducing Yeast NDI1 Gene
CONCLUSIONS: NDI1 compensates for the defective complex I in MPP+/MPTP-induced models, and vastly alleviates MPTP-induced toxic effect on dopaminergic neurons. Our study may provide a basis for gene therapy of sporadic PD with defective complex I caused by MPTP-like substance.PMID:38594619 | PMC:PMC11003148 | DOI:10.1186/s12575-024-00236-3 (Source: Biological Procedures Online)
Source: Biological Procedures Online - April 9, 2024 Category: Molecular Biology Authors: Hongzhi Li Jing Zhang Yuqi Shen Yifan Ye Qingyou Jiang Lan Chen Bohao Sun Zhuo Chen Luxi Shen Hezhi Fang Jifeng Yang Haihua Gu Source Type: research
Targeting Mitochondrial Complex I Deficiency in MPP < sup > + < /sup > /MPTP-induced Parkinson's Disease Cell Culture and Mouse Models by Transducing Yeast NDI1 Gene
CONCLUSIONS: NDI1 compensates for the defective complex I in MPP+/MPTP-induced models, and vastly alleviates MPTP-induced toxic effect on dopaminergic neurons. Our study may provide a basis for gene therapy of sporadic PD with defective complex I caused by MPTP-like substance.PMID:38594619 | PMC:PMC11003148 | DOI:10.1186/s12575-024-00236-3 (Source: Biological Procedures Online)
Source: Biological Procedures Online - April 9, 2024 Category: Molecular Biology Authors: Hongzhi Li Jing Zhang Yuqi Shen Yifan Ye Qingyou Jiang Lan Chen Bohao Sun Zhuo Chen Luxi Shen Hezhi Fang Jifeng Yang Haihua Gu Source Type: research
Alleviating Neurodegenerative Diseases Associated with Mitochondrial Defects by Therapeutic Biomolecules
Curr Top Med Chem. 2024 Apr 5. doi: 10.2174/0115680266299148240329062647. Online ahead of print.ABSTRACTNeurodegenerative diseases are emerging as a global health concern in the current sce-nario, and their association with mitochondrial defects has been a potential area of research. Mi-tochondria, one of the essential organelles of the cell, serve as the cell's powerhouse, producing energy and ensuring cellular health. Neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis, and Pelizaeus-Merzbacher disease have been found to be primarily triggered by mitochondrial malfunct...
Source: Current Topics in Medicinal Chemistry - April 9, 2024 Category: Chemistry Authors: Tanmoy Roy Swarupanjali Padhi Rupa Mazumder Chandana Majee Saumya Das Monika Monika Rashmi Mishra Bhupinder Kapoor Source Type: research
Targeting Mitochondrial Complex I Deficiency in MPP < sup > + < /sup > /MPTP-induced Parkinson's Disease Cell Culture and Mouse Models by Transducing Yeast NDI1 Gene
CONCLUSIONS: NDI1 compensates for the defective complex I in MPP+/MPTP-induced models, and vastly alleviates MPTP-induced toxic effect on dopaminergic neurons. Our study may provide a basis for gene therapy of sporadic PD with defective complex I caused by MPTP-like substance.PMID:38594619 | PMC:PMC11003148 | DOI:10.1186/s12575-024-00236-3 (Source: Biological Procedures Online)
Source: Biological Procedures Online - April 9, 2024 Category: Molecular Biology Authors: Hongzhi Li Jing Zhang Yuqi Shen Yifan Ye Qingyou Jiang Lan Chen Bohao Sun Zhuo Chen Luxi Shen Hezhi Fang Jifeng Yang Haihua Gu Source Type: research
The role of mesenchymal stem cells in early programming of adipose tissue in the offspring of women with obesity
In conclusion, maternal obesity can induce early programming of fetal adipose tissue by conditioning MSCs. These cells have higher expression of adipogenic markers, altered insulin signalling and mitochondrial performance, compared to MSCs of neonates from lean pregnancies. Fetal MSCs imprinting by maternal obesity could help explain the increased risk of childhood obesity and development of further noncommunicable diseases. (Source: Pediatric Obesity)
Source: Pediatric Obesity - April 9, 2024 Category: Eating Disorders & Weight Management Authors: Sof ía Bellalta,
Torsten Plösch,
Marijke Faas,
Paola Casanello Tags: REVIEW ARTICLE Source Type: research
The requirement of the mitochondrial protein NDUFS8 for angiogenesis
Cell Death & Disease, Published online: 09 April 2024; doi:10.1038/s41419-024-06636-3The requirement of the mitochondrial protein NDUFS8 for angiogenesis (Source: Cell death and disease)
Source: Cell death and disease - April 9, 2024 Category: Internal Medicine Authors: Qian-wei Xiong Kun Jiang Xiao-wei Shen Zhou-rui Ma Xiang-ming Yan Hao Xia Xu Cao Source Type: research
Potential Applications of Mitochondrial Therapy with a Focus on Parkinson's Disease and Mitochondrial Transplantation
CONCLUSION: The development of innovative therapeutics for mitochondria-directed treatments in Parkinson's disease may be aided by optimizing mitochondrial dynamics. Many neurological diseases have been studied in animal and cellular models, and it has been found that mitochondrial maintenance can slow the death of neuronal cells. It has been hypothesized that drug therapies for neurodegenerative diseases that focus on mitochondrial dysfunction will help to delay the onset of neuronal dysfunction.PMID:38585467 | PMC:PMC10997929 | DOI:10.34172/apb.2024.019 (Source: Adv Data)
Source: Adv Data - April 8, 2024 Category: Epidemiology Authors: Pranay Wal Ankita Wal Himangi Vig Danish Mahmood Mohd Masih Uzzaman Khan Source Type: research
G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1-Bax-mediated mitochondrial apoptosis pathway
CONCLUSION: Our study showed that the G6PD-VDAC1-Bax axis is a vital switch in VSMC apoptosis and is essential for VSMC phenotypic switching and neointimal hyperplasia, providing mechanistic insight into early VRDs.PMID:38589823 | DOI:10.1186/s11658-024-00566-w (Source: Cellular and Molecular Biology Letters)
Source: Cellular and Molecular Biology Letters - April 8, 2024 Category: Biochemistry Authors: Ting Zhang Rui-Jie Cao Jiang-Ling Niu Zhi-Huan Chen Shi-Qing Mu Tong Cao Jie-Xin Pang Li-Hua Dong Source Type: research
G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1-Bax-mediated mitochondrial apoptosis pathway
CONCLUSION: Our study showed that the G6PD-VDAC1-Bax axis is a vital switch in VSMC apoptosis and is essential for VSMC phenotypic switching and neointimal hyperplasia, providing mechanistic insight into early VRDs.PMID:38589823 | DOI:10.1186/s11658-024-00566-w (Source: Mol Biol Cell)
Source: Mol Biol Cell - April 8, 2024 Category: Molecular Biology Authors: Ting Zhang Rui-Jie Cao Jiang-Ling Niu Zhi-Huan Chen Shi-Qing Mu Tong Cao Jie-Xin Pang Li-Hua Dong Source Type: research
Cardiac-specific deletion of heat shock protein 60 induces mitochondrial stress and disrupts heart development in mice
Biochem Biophys Res Commun. 2024 Apr 4;710:149883. doi: 10.1016/j.bbrc.2024.149883. Online ahead of print.ABSTRACTCongenital heart diseases are the most common birth defects around the world. Emerging evidence suggests that mitochondrial homeostasis is required for normal heart development. In mitochondria, a series of molecular chaperones including heat shock protein 60 (HSP60) are engaged in assisting the import and folding of mitochondrial proteins. However, it remains largely obscure whether and how these mitochondrial chaperones regulate cardiac development. Here, we generated a cardiac-specific Hspd1 deletion mouse m...
Source: Biochemical and Biophysical Research communications - April 8, 2024 Category: Biochemistry Authors: Tao Shen Shuting Wang Can Huang Siting Zhu Xiangbin Zhu Na Li Hong Wang Lei Huang Mingming Ren Zhen Han Jianjun Ge Ze'e Chen Kunfu Ouyang Source Type: research
Potential Applications of Mitochondrial Therapy with a Focus on Parkinson's Disease and Mitochondrial Transplantation
CONCLUSION: The development of innovative therapeutics for mitochondria-directed treatments in Parkinson's disease may be aided by optimizing mitochondrial dynamics. Many neurological diseases have been studied in animal and cellular models, and it has been found that mitochondrial maintenance can slow the death of neuronal cells. It has been hypothesized that drug therapies for neurodegenerative diseases that focus on mitochondrial dysfunction will help to delay the onset of neuronal dysfunction.PMID:38585467 | PMC:PMC10997929 | DOI:10.34172/apb.2024.019 (Source: Adv Data)
Source: Adv Data - April 8, 2024 Category: Epidemiology Authors: Pranay Wal Ankita Wal Himangi Vig Danish Mahmood Mohd Masih Uzzaman Khan Source Type: research
G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1-Bax-mediated mitochondrial apoptosis pathway
CONCLUSION: Our study showed that the G6PD-VDAC1-Bax axis is a vital switch in VSMC apoptosis and is essential for VSMC phenotypic switching and neointimal hyperplasia, providing mechanistic insight into early VRDs.PMID:38589823 | PMC:PMC11003121 | DOI:10.1186/s11658-024-00566-w (Source: Mol Biol Cell)
Source: Mol Biol Cell - April 8, 2024 Category: Molecular Biology Authors: Ting Zhang Rui-Jie Cao Jiang-Ling Niu Zhi-Huan Chen Shi-Qing Mu Tong Cao Jie-Xin Pang Li-Hua Dong Source Type: research
Cardiac-specific deletion of heat shock protein 60 induces mitochondrial stress and disrupts heart development in mice
Biochem Biophys Res Commun. 2024 Apr 4;710:149883. doi: 10.1016/j.bbrc.2024.149883. Online ahead of print.ABSTRACTCongenital heart diseases are the most common birth defects around the world. Emerging evidence suggests that mitochondrial homeostasis is required for normal heart development. In mitochondria, a series of molecular chaperones including heat shock protein 60 (HSP60) are engaged in assisting the import and folding of mitochondrial proteins. However, it remains largely obscure whether and how these mitochondrial chaperones regulate cardiac development. Here, we generated a cardiac-specific Hspd1 deletion mouse m...
Source: Biochemical and Biophysical Research communications - April 8, 2024 Category: Biochemistry Authors: Tao Shen Shuting Wang Can Huang Siting Zhu Xiangbin Zhu Na Li Hong Wang Lei Huang Mingming Ren Zhen Han Jianjun Ge Ze'e Chen Kunfu Ouyang Source Type: research
G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1-Bax-mediated mitochondrial apoptosis pathway
CONCLUSION: Our study showed that the G6PD-VDAC1-Bax axis is a vital switch in VSMC apoptosis and is essential for VSMC phenotypic switching and neointimal hyperplasia, providing mechanistic insight into early VRDs.PMID:38589823 | PMC:PMC11003121 | DOI:10.1186/s11658-024-00566-w (Source: Cellular and Molecular Biology Letters)
Source: Cellular and Molecular Biology Letters - April 8, 2024 Category: Biochemistry Authors: Ting Zhang Rui-Jie Cao Jiang-Ling Niu Zhi-Huan Chen Shi-Qing Mu Tong Cao Jie-Xin Pang Li-Hua Dong Source Type: research
An externally validated clinical-laboratory nomogram for myocardial involvement in adult idiopathic-inflammatory-myopathy patients
ConclusionThis study developed and validated a nomogram model to predict the risk of MI in adult IIMs patients, which can benefit the prediction and early identification of MI as well as timely intervention in these patients. (Source: Clinical Rheumatology)
Source: Clinical Rheumatology - April 8, 2024 Category: Rheumatology Source Type: research
