Type 2 diabetes mellitus and cardiovascular disease: Genetic and epigenetic links
Open accessAbstract
Type 2 diabetes mellitus (DM) is a common metabolic disorder predisposing to diabetic cardiomyopathy and atherosclerotic cardiovascular disease (CVD), which could lead to heart failure through a variety of mechanisms, including myocardial infarction and chronic pressure overload. Pathogenetic mechanisms, mainly linked to hyperglycemia and chronic sustained hyperinsulinemia, include changes in metabolic profiles, intracellular signaling pathways, energy production, redox status, increased susceptibility to ischemia, and extracellular matrix remodeling. The close relationship between type 2 DM and CVD has led to the common soil hypothesis, postulating that both conditions share common genetic and environmental factors influencing this association. However, although the common risk factors of both CVD and type 2 DM, such as obesity, insulin resistance, dyslipidemia, inflammation, and thrombophilia, can be identified in the majority of affected patients, less is known about how these factors influence both conditions, so that efforts are still needed for a more comprehensive understanding of this relationship. The genetic, epigenetic, and environmental backgrounds of both type 2 DM and CVD have been more recently studied and updated. However, the underlying pathogenetic mechanisms have seldom been investigated within the broader shared background, but rather studied in the specific context of type 2 DM or CVD, separately. As the precise pathophysiological links between type 2 DM and CVD are not entirely understood and many aspects still require elucidation, an integrated description of the genetic, epigenetic, and environmental influences involved in the concomitant development of both diseases is of paramount importance to shed new light on the interlinks between type 2 DM and CVD. This review addresses the current knowledge of overlapping genetic and epigenetic aspects in type 2 DM and CVD, including microRNAs and long non-coding RNAs, whose abnormal regulation has been implicated in both disease conditions, either etiologically or as cause for their progression. Understanding the links between these disorders may help to drive future research toward an integrated pathophysiological approach and to provide future directions in the field.
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HMGA1 is a master regulator of the vascular SMC phenotypic switch following vessel wall injury and release of proinflammatory cytokines.
“The architectural transcription factor HMGA1 is a master regulator of the vascular SMCs phenotypic switch that follows vessel wall injury and release of proinflammatory cytokines [6,190,191].”
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The Association between HMGA1 rs146052672 Variant and Type 2 Diabetes: A Transethnic Meta-Analysis
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Flagged first, then by citations
Research works printed but not linked: 1
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Mediterranean diet nutrients to turn the tide against insulin resistance and related diseases
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The Diabetic Cardiomyopathy: The Contributing Pathophysiological Mechanisms
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Cellular senescence links aging and diabetes in cardiovascular disease
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Hassanzadeh-Rostami, Z., Hemmatdar, Z., Pishdad, G. R., & Faghih, S. (2021) · Experimental and Clinical Endocrinology & Diabetes · doi:10.1055/a-0929-6287 · Cited by 22 · see citing works
- Authors
- De Rosa, S., Arcidiacono, B., Chiefari, E., Brunetti, A., Indolfi, C., & Foti, D. P.
- Affiliations
- Magna Graecia University (IT)
- Corresponding author
- Brunetti, Antonio
- Indolfi, Ciro
- Foti, Daniela P.
- Venue
- Frontiers in Endocrinology
- Publisher
- Frontiers Media SA
- Published
- 2018-01-17
- Volume
- 9
- Pages
- 2-2
- ISSN
- 1664-2392 (ISSN-L)
- PMC
- PMC5776102
- OpenAlex
- W2783270596
- Cited by
- 369
- References
- 199
- Citations by year
- 2026: 20 · 2025: 44 · 2024: 50 · 2023: 56 · 2022: 46 · 2021: 46 · 2020: 42 · 2019: 42 · 2018: 23
- FWCI
- 5.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Endocrinology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Archive of Doctoral Theses and Digital Collections (University of Calabria) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- type 2 diabetes, cardiovascular disease, diabetic cardiomyopathy, atherosclerosis, heart failure, genetic susceptibility, epigenetics, microRNA, long non-coding RNA, hyperglycemia, hyperinsulinemia, insulin resistance, obesity, inflammation, thrombophilia, extracellular matrix remodeling, redox state
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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