Environment, Genetics, and Cardiovascular Disease

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (30 November 2025) | Viewed by 1307

Special Issue Editor

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD) remains the leading cause of death worldwide, responsible for approximately 18 million deaths each year. Over the past century, our understanding of the significance of modifiable risk factors—such as diet, physical activity, and smoking—has advanced dramatically. Concurrently, exposure to environmental pollutants, whether in the air, water, or physical surroundings, is increasingly acknowledged as a critical, yet often overlooked, contributor to CVD. 

Furthermore, our comprehension of the mechanisms by which these environmental toxicants contribute to CVD remains limited. The quote, “genetics loads the gun, but the environment pulls the trigger,” aptly illustrates the complex interplay between CVD and environmental influences. Environmental exposures can amplify or mitigate the effects of genetic susceptibility, while genetic factors can also influence how individuals respond to environmental risks.

We invite researchers to submit original research and review articles for this Special Issue, which aims to explore the intricate relationship between environmental factors and CVD, with a particular focus on how these external influences interact with genetic predispositions

Dr. Andrea Borghini
Guest Editor

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Keywords

  • cardiovascular disease
  • environmental exposure
  • genetics
  • epigenetics

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Published Papers (1 paper)

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Review

39 pages, 2256 KB  
Review
From Exposure to Atherosclerosis: Mechanistic Insights into Phthalate-Driven Ischemic Heart Disease and Prevention Strategies
by Francesca Gorini, Alessandro Tonacci, Mariangela Palazzo and Andrea Borghini
Life 2026, 16(2), 327; https://doi.org/10.3390/life16020327 - 13 Feb 2026
Viewed by 874
Abstract
Despite decades of interventions targeting modifiable risk factors to reduce the burden of cardiovascular disease, ischemic heart disease (IHD) remains the leading cause of mortality and the second leading cause of disability-adjusted life-years worldwide. Growing evidence suggests that phthalates–plasticizers widely used in consumer [...] Read more.
Despite decades of interventions targeting modifiable risk factors to reduce the burden of cardiovascular disease, ischemic heart disease (IHD) remains the leading cause of mortality and the second leading cause of disability-adjusted life-years worldwide. Growing evidence suggests that phthalates–plasticizers widely used in consumer products, cosmetics, and medical devices, and therefore ubiquitous across environmental media, may contribute to IHD development. Epidemiological studies have reported associations between phthalate exposure and multiple markers of atherosclerosis, the pathological hallmark of IHD, with or without mediation by traditional cardiovascular risk factors. Experimental models support these findings, showing that phthalates can induce oxidative stress, mitochondrial dysfunction, apoptosis, lipid accumulation, and epigenetic alterations, all of which promote endothelial damage and atherogenesis. In this review, we synthesize current epidemiological findings linking phthalate exposure to IHD, describe the main cellular and molecular mechanisms involved, and outline research gaps and regulatory perspectives. We also discuss how novel analytical frameworks—including artificial intelligence—may enhance the integration of environmental, clinical, and molecular data to advance risk prediction and prevention strategies. Full article
(This article belongs to the Special Issue Environment, Genetics, and Cardiovascular Disease)
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