The DOI matches its Crossref record, with a small difference in title or year; 56 of the 56 references it cites were found in a registry or an index.
The Pathobiology of Diabetic Complications
Abstract
It’s a great honor to join the exceptional club of Banting Award winners, many of whom were my role models and mentors. In addition, giving the Banting Lecture also has a very personal meaning to me, because without Frederick Banting, I would have died from type 1 diabetes when I was 8 years old. However, it was already apparent at the time I was diagnosed that for too many people like me, Banting’s discovery of insulin only allowed them to live just long enough to develop blindness, renal failure, and coronary disease. For example, when I started college, the American Diabetes Association’s Diabetes Textbook had this to say to my parents: “The person with type 1 diabetes can be reassured that it is highly likely that he will live at least into his 30s.” Not surprisingly, my parents did not find this particularly reassuring. At the same time we were reading this in 1967, however, the first basic research discovery about the pathobiology of diabetic complications had just been published in Science the previous year. In my Banting Lecture today, I am thus going to tell you a scientific story that is also profoundly personal. I’ve divided my talk into three parts. The first part is called “pieces of the puzzle,” and in it I describe what was learned about the pathobiology of diabetic complications starting with that 1966 Science paper and continuing through the end of the 1990s. In the second part, I present a unified mechanism that links together all of the seemingly unconnected pieces of the puzzle. Finally, in the third part, I focus on three examples of novel therapeutic approaches for the prevention and treatment of diabetic complications, which are all based on the new paradigm of a unifying mechanism for the pathogenesis of diabetic complications. …
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“hyperglycemia has been shown to increase mitochondrial ROS production in endothelial cells (28), as well as in other cell types (29).”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [28]
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Metadata
- Authors
- Brownlee, M.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Brownlee, Michael
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-06-01
- Volume
- 54
- Issue
- 6
- Pages
- 1615-1625
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2471605942
- Cited by
- 5,339
- References
- 56
- Citations by year
- 2026: 286 · 2025: 248 · 2024: 230 · 2023: 233 · 2022: 299 · 2021: 310 · 2020: 309 · 2019: 295 · 2018: 279 · 2017: 278 · 2016: 281 · 2015: 305 · 2014: 349 · 2013: 294 · 2012: 275
- FWCI
- 90.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- diabetes complications, pathobiology, type 1 diabetes, diabetic nephropathy, diabetic retinopathy, diabetic cardiovascular disease, insulin
- MeSH terms
- Animals, Humans, Hyperglycemia, Mitochondria, Diabetes Complications
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