Difference between revisions of "Brownlee 2001 Nature"
From Bioblast
Line 1: | Line 1: | ||
{{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 | ||
Line 7: | Line 7: | ||
|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. | ||
}} | }} | ||
[[File:Brownlee 2001 Nature CORRECTION.png|right|400px]] | |||
ย | {{Template:Correction FADH2 and S-pathway}} | ||
{{ | |||
}} |
Revision as of 17:57, 19 March 2023
Brownlee M (2001) Biochemistry and molecular cell biology of diabetic complications. Nature 14:813-20. doi: 10.1038/414813a |
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.
Correction: FADH2 and Complex II
- 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