ROS networks: designs, aging, Parkinson’s disease and precision therapies

How the network around ROS protects against oxidative stress and Parkinson’s disease (PD), and how processes at the minutes timescale cause disease and aging after decades, remains enigmatic. Challenging whether the ROS network is as complex as it seems, we built a fairly comprehensive version there...

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Published inNPJ systems biology and applications Vol. 6; no. 1; p. 34
Main Authors N. Kolodkin, Alexey, Sharma, Raju Prasad, Colangelo, Anna Maria, Ignatenko, Andrew, Martorana, Francesca, Jennen, Danyel, Briedé, Jacco J., Brady, Nathan, Barberis, Matteo, Mondeel, Thierry D. G. A., Papa, Michele, Kumar, Vikas, Peters, Bernhard, Skupin, Alexander, Alberghina, Lilia, Balling, Rudi, Westerhoff, Hans V.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 26.10.2020
Nature Publishing Group
Subjects
631/553/2695
631/553/2700
631/553/2703
631/553/2710
631/553/2717
Aging
Antioxidants
Bioinformatics
Biomedical and Life Sciences
Caffeine
Computational Biology
Computational Biology/Bioinformatics
Computer Appl. in Life Sciences
Humans
Life Sciences
Mitochondria
Models, Biological
Molecular Targeted Therapy
Movement disorders
Neurodegenerative diseases
Oxidative Stress
PARK7 protein
Parkinson Disease - metabolism
Parkinson Disease - physiopathology
Parkinson Disease - therapy
Parkinson's disease
Precision Medicine
Reactive Oxygen Species - metabolism
Synuclein
Systems Biology
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Abstract How the network around ROS protects against oxidative stress and Parkinson’s disease (PD), and how processes at the minutes timescale cause disease and aging after decades, remains enigmatic. Challenging whether the ROS network is as complex as it seems, we built a fairly comprehensive version thereof which we disentangled into a hierarchy of only five simpler subnetworks each delivering one type of robustness. The comprehensive dynamic model described in vitro data sets from two independent laboratories. Notwithstanding its five-fold robustness, it exhibited a relatively sudden breakdown, after some 80 years of virtually steady performance: it predicted aging. PD-related conditions such as lack of DJ-1 protein or increased α-synuclein accelerated the collapse, while antioxidants or caffeine retarded it. Introducing a new concept (aging-time-control coefficient), we found that as many as 25 out of 57 molecular processes controlled aging. We identified new targets for “life-extending interventions”: mitochondrial synthesis, KEAP1 degradation, and p62 metabolism.
AbstractList How the network around ROS protects against oxidative stress and Parkinson’s disease (PD), and how processes at the minutes timescale cause disease and aging after decades, remains enigmatic. Challenging whether the ROS network is as complex as it seems, we built a fairly comprehensive version thereof which we disentangled into a hierarchy of only five simpler subnetworks each delivering one type of robustness. The comprehensive dynamic model described in vitro data sets from two independent laboratories. Notwithstanding its five-fold robustness, it exhibited a relatively sudden breakdown, after some 80 years of virtually steady performance: it predicted aging. PD-related conditions such as lack of DJ-1 protein or increased α-synuclein accelerated the collapse, while antioxidants or caffeine retarded it. Introducing a new concept (aging-time-control coefficient), we found that as many as 25 out of 57 molecular processes controlled aging. We identified new targets for “life-extending interventions”: mitochondrial synthesis, KEAP1 degradation, and p62 metabolism.
How the network around ROS protects against oxidative stress and Parkinson's disease (PD), and how processes at the minutes timescale cause disease and aging after decades, remains enigmatic. Challenging whether the ROS network is as complex as it seems, we built a fairly comprehensive version thereof which we disentangled into a hierarchy of only five simpler subnetworks each delivering one type of robustness. The comprehensive dynamic model described in vitro data sets from two independent laboratories. Notwithstanding its five-fold robustness, it exhibited a relatively sudden breakdown, after some 80 years of virtually steady performance: it predicted aging. PD-related conditions such as lack of DJ-1 protein or increased α-synuclein accelerated the collapse, while antioxidants or caffeine retarded it. Introducing a new concept (aging-time-control coefficient), we found that as many as 25 out of 57 molecular processes controlled aging. We identified new targets for "life-extending interventions": mitochondrial synthesis, KEAP1 degradation, and p62 metabolism.How the network around ROS protects against oxidative stress and Parkinson's disease (PD), and how processes at the minutes timescale cause disease and aging after decades, remains enigmatic. Challenging whether the ROS network is as complex as it seems, we built a fairly comprehensive version thereof which we disentangled into a hierarchy of only five simpler subnetworks each delivering one type of robustness. The comprehensive dynamic model described in vitro data sets from two independent laboratories. Notwithstanding its five-fold robustness, it exhibited a relatively sudden breakdown, after some 80 years of virtually steady performance: it predicted aging. PD-related conditions such as lack of DJ-1 protein or increased α-synuclein accelerated the collapse, while antioxidants or caffeine retarded it. Introducing a new concept (aging-time-control coefficient), we found that as many as 25 out of 57 molecular processes controlled aging. We identified new targets for "life-extending interventions": mitochondrial synthesis, KEAP1 degradation, and p62 metabolism.
ArticleNumber 34
Author Peters, Bernhard
Mondeel, Thierry D. G. A.
Westerhoff, Hans V.
Kumar, Vikas
Briedé, Jacco J.
Colangelo, Anna Maria
Martorana, Francesca
Skupin, Alexander
Alberghina, Lilia
Brady, Nathan
Sharma, Raju Prasad
Papa, Michele
Barberis, Matteo
Ignatenko, Andrew
Balling, Rudi
N. Kolodkin, Alexey
Jennen, Danyel
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Snippet How the network around ROS protects against oxidative stress and Parkinson’s disease (PD), and how processes at the minutes timescale cause disease and aging...
How the network around ROS protects against oxidative stress and Parkinson's disease (PD), and how processes at the minutes timescale cause disease and aging...
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StartPage 34
SubjectTerms 631/553/2695
631/553/2700
631/553/2703
631/553/2710
631/553/2717
Aging
Antioxidants
Bioinformatics
Biomedical and Life Sciences
Caffeine
Computational Biology
Computational Biology/Bioinformatics
Computer Appl. in Life Sciences
Humans
Life Sciences
Mitochondria
Models, Biological
Molecular Targeted Therapy
Movement disorders
Neurodegenerative diseases
Oxidative Stress
PARK7 protein
Parkinson Disease - metabolism
Parkinson Disease - physiopathology
Parkinson Disease - therapy
Parkinson's disease
Precision Medicine
Reactive Oxygen Species - metabolism
Synuclein
Systems Biology
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Title ROS networks: designs, aging, Parkinson’s disease and precision therapies
URI https://link.springer.com/article/10.1038/s41540-020-00150-w
https://www.ncbi.nlm.nih.gov/pubmed/33106503
https://www.proquest.com/docview/2471521866
https://www.proquest.com/docview/2454653859
https://pubmed.ncbi.nlm.nih.gov/PMC7589522
Volume 6
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