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Difference between revisions of "Brownlee 2001 Nature"

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{{Publication
{{Publication
|title=Brownlee M (2001) Biochemistry and molecular cell biology of diabetic complications. Nature 14:813-20.
|title=Brownlee M (2001) Biochemistry and molecular cell biology of diabetic complications. Nature 14:813-20. doi: 10.1038/414813a
|info=[https://pubmed.ncbi.nlm.nih.gov/11742414/ PMID:11742414]
|info=[https://pubmed.ncbi.nlm.nih.gov/11742414/ PMID:11742414 Open Access]
|authors=Brownlee M
|authors=Brownlee M
|year=2001
|year=2001
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|abstract=Diabetes-specific microvascular disease is a leading cause of blindness, renal failure and nerve damage, and diabetes-accelerated atherosclerosis leads to increased risk of myocardial infarction, stroke and limb amputation. Four main molecular mechanisms have been implicated in glucose-mediated vascular damage. All seem to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain. This integrating paradigm provides a new conceptual framework for future research and drug discovery.
|abstract=Diabetes-specific microvascular disease is a leading cause of blindness, renal failure and nerve damage, and diabetes-accelerated atherosclerosis leads to increased risk of myocardial infarction, stroke and limb amputation. Four main molecular mechanisms have been implicated in glucose-mediated vascular damage. All seem to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain. This integrating paradigm provides a new conceptual framework for future research and drug discovery.
}}
}}
== Cited by ==
[[File:Brownlee 2001 Nature CORRECTION.png|right|400px]]
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{{Template:Correction FADH2 and S-pathway}}
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Revision as of 17:57, 19 March 2023

Publications in the MiPMap
Brownlee M (2001) Biochemistry and molecular cell biology of diabetic complications. Nature 14:813-20. doi: 10.1038/414813a

ยป PMID:11742414 Open Access

Brownlee M (2001) Nature

Abstract: Diabetes-specific microvascular disease is a leading cause of blindness, renal failure and nerve damage, and diabetes-accelerated atherosclerosis leads to increased risk of myocardial infarction, stroke and limb amputation. Four main molecular mechanisms have been implicated in glucose-mediated vascular damage. All seem to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain. This integrating paradigm provides a new conceptual framework for future research and drug discovery.

Brownlee 2001 Nature CORRECTION.png

Correction: FADH2 and Complex II

Ambiguity alert.png
FADH2 is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2024).
Gnaiger E (2024) Complex II ambiguities โ€• FADH2 in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - ยปBioblast linkยซ