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The changing epidemiology of human type 2 diabetes–associated atherosclerosis : Pathophysiological mechanisms and emerging treatment possibilities

Al-Sharify, Dania LU orcid ; Sun, Jiangming LU orcid and Edsfeldt, Andreas LU orcid (2026) In Journal of Internal Medicine 300(2). p.131-152
Abstract

Type 2 diabetes (T2D) is a major global health concern strongly associated with atherosclerosis and subsequent macrovascular complications. These complications are the leading cause of death among T2D patients. Despite a decline in cardiovascular events over the last decade, individuals with T2D still have an approximately doubled risk compared to those without diabetes. This shows an urgent need for therapies targeting biological processes specific to T2D-associated atherosclerosis. Nevertheless, more research is needed to identify exactly which processes can be targeted therapeutically. Current therapies either target lipid metabolism or inflammation, two processes commonly considered important in T2D-associated atherosclerosis.... (More)

Type 2 diabetes (T2D) is a major global health concern strongly associated with atherosclerosis and subsequent macrovascular complications. These complications are the leading cause of death among T2D patients. Despite a decline in cardiovascular events over the last decade, individuals with T2D still have an approximately doubled risk compared to those without diabetes. This shows an urgent need for therapies targeting biological processes specific to T2D-associated atherosclerosis. Nevertheless, more research is needed to identify exactly which processes can be targeted therapeutically. Current therapies either target lipid metabolism or inflammation, two processes commonly considered important in T2D-associated atherosclerosis. However, more recent human plaque tissue studies show no differences in plaque levels of lipids nor inflammatory markers, possibly reflecting improved clinical treatment strategies. Other distinct differences in plaque tissue composition in T2D have been put forward, including thin fibrous caps and large necrotic cores. Moreover, T2D may influence several biological processes affecting both plaque formation and progression (such as oxidative stress and efferocytosis). These mechanisms could potentially also be targeted to prevent atherosclerotic cardiovascular complications. This review focuses on the shifting epidemiology of T2D-associated cardiovascular complications, as well as biological changes in T2D plaques, and how these changes can guide future clinical approaches to further reduce atherosclerotic complications.

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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
atherosclerosis, cardiovascular complications, genetics, imaging, therapies, type 2 diabetes
in
Journal of Internal Medicine
volume
300
issue
2
pages
131 - 152
publisher
Wiley-Blackwell
external identifiers
  • scopus:105041527359
  • pmid:42286930
ISSN
0954-6820
DOI
10.1111/joim.70118
language
English
LU publication?
yes
additional info
Publisher Copyright: © 2026 The Author(s). Journal of Internal Medicine published by John Wiley & Sons Ltd on behalf of Association for Publication of The Journal of Internal Medicine.
id
6ea75b23-a82b-48dd-94da-559e94af3a5d
date added to LUP
2026-08-11 13:46:17
date last changed
2026-08-12 03:09:23
@article{6ea75b23-a82b-48dd-94da-559e94af3a5d,
  abstract     = {{<p>Type 2 diabetes (T2D) is a major global health concern strongly associated with atherosclerosis and subsequent macrovascular complications. These complications are the leading cause of death among T2D patients. Despite a decline in cardiovascular events over the last decade, individuals with T2D still have an approximately doubled risk compared to those without diabetes. This shows an urgent need for therapies targeting biological processes specific to T2D-associated atherosclerosis. Nevertheless, more research is needed to identify exactly which processes can be targeted therapeutically. Current therapies either target lipid metabolism or inflammation, two processes commonly considered important in T2D-associated atherosclerosis. However, more recent human plaque tissue studies show no differences in plaque levels of lipids nor inflammatory markers, possibly reflecting improved clinical treatment strategies. Other distinct differences in plaque tissue composition in T2D have been put forward, including thin fibrous caps and large necrotic cores. Moreover, T2D may influence several biological processes affecting both plaque formation and progression (such as oxidative stress and efferocytosis). These mechanisms could potentially also be targeted to prevent atherosclerotic cardiovascular complications. This review focuses on the shifting epidemiology of T2D-associated cardiovascular complications, as well as biological changes in T2D plaques, and how these changes can guide future clinical approaches to further reduce atherosclerotic complications.</p>}},
  author       = {{Al-Sharify, Dania and Sun, Jiangming and Edsfeldt, Andreas}},
  issn         = {{0954-6820}},
  keywords     = {{atherosclerosis; cardiovascular complications; genetics; imaging; therapies; type 2 diabetes}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{131--152}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Journal of Internal Medicine}},
  title        = {{The changing epidemiology of human type 2 diabetes–associated atherosclerosis : Pathophysiological mechanisms and emerging treatment possibilities}},
  url          = {{http://dx.doi.org/10.1111/joim.70118}},
  doi          = {{10.1111/joim.70118}},
  volume       = {{300}},
  year         = {{2026}},
}