Organoids—three-dimensional structures derived from stem cells—are transforming biomedical research by modeling key aspects of human physiology and disease. By replicating native tissue architecture, cellular heterogeneity, and functional behavior, they provide human-relevant systems that address limitations inherent to conventional in-vitro and animal models.

Diabetes and cardiovascular disease are deeply interconnected conditions, characterized by shared, multi-organ pathophysiology. Organoid technologies offer unique opportunities to dissect disease mechanisms, evaluate therapeutic strategies, and develop personalized, physiologically relevant models. These systems enable the investigation of cardiometabolic processes in platforms that better reflect the complexity and progression of human disease.

Cardiovascular Diabetology welcomes original research articles, reviews, and meta-analyses for this Collection, which aims to highlight the use of organoid technologies in advancing our understanding of cardiovascular complications associated with diabetes.

Areas of interest include, but are not limited to:

- Organoid models of diabetic cardiomyopathy and heart failure

- Matrigel alternatives for organoid development

- Cell-cell and extracellular matrix interactions in organoids

- Organoid-based drug testing for cardiovascular diseases

- Organoid-on-chip systems for tissue crosstalk and perfusion3D bioprinting and tissue engineering for cardiovascular organoids

- Artificial intelligence–driven analysis of organoid function and phenotypes

- Organoid models of gestational diabetes–induced congenital heart disease

- Functional genomics using CRISPR in cardiovascular organoids

- Single-cell and spatial omics to map disease states in organoids

- Co-culture systems of vascular and pancreatic organoids to study metabolic-vascular crosstalk

- Organoid-based screening platforms for anti-diabetic and cardioprotective drugs

Submissions that contribute to conceptual clarity (e.g., distinctions between organoids and spheroids), incorporate multi-organ or metabolic system perspectives, or connect technological development with clinical or translational insights are especially welcome.

This Collection supports and amplifies research related to SDG 3, Good Health and Well-Being.

All submissions in this collection undergo the journal’s standard peer review process. Similarly, all manuscripts authored by a Guest Editor(s) will be handled by the Editor-in-Chief. As an open access publication, this journal levies an article processing fee (details here). We recognize that many key stakeholders may not have access to such resources and are committed to supporting participation in this issue wherever resources are a barrier. For more information about what support may be available, please visit OA funding and support, or email OAfundingpolicy@springernature.com or the Editor-in-Chief.

Cardiometabolic and liver diseases are no longer viewed as isolated entities. Growing evidence shows that hepatic and cardiovascular dysfunctions are tightly interconnected through shared metabolic, inflammatory, hemodynamic, and hormonal pathways. This crosstalk shapes disease trajectories and opens opportunities for integrated diagnostics and therapies.

Key interconnections include:

- Insulin resistance. The liver is pivotal for glucose and lipid homeostasis. Hepatic insulin resistance drives excess glucose production and dyslipidemia, contributing to the cardiovascular–kidney–metabolic (CKM) syndrome.

- Metabolic dysfunction–associated steatotic liver disease (MASLD). Highly prevalent in obesity and metabolic syndrome, and especially common in type 2 diabetes (T2D), which bears the highest MASLD burden. Progression to steatohepatitis or fibrosis markedly increases atherosclerotic risk.

- Liver-derived factors. Hepatokines (e.g., FGF21) and extracellular vesicles influence cardiac tissue, vascular tone, and systemic metabolism, potentially amplifying inflammation, oxidative stress, and lipotoxicity across organs.

- Systemic inflammation and lipotoxicity. Visceral adipose tissue and the liver release inflammatory cytokines and triglyceride-rich lipids, promoting endothelial dysfunction and perpetuating metabolic disturbances.

- Dyslipidemia. Elevated triglycerides and LDL, with reduced HDL, accelerate atherogenesis and cardiovascular risk.

- Hemodynamic and metabolic stress. Heart failure can cause hepatic congestion and hypoperfusion, while advanced liver disease can precipitate cirrhotic cardiomyopathy and arrhythmias, even in the absence of prior heart failure.

In summary, hepatic and cardiometabolic systems are functionally and pathologically intertwined: liver dysfunction worsens cardiovascular and metabolic health, and cardiometabolic disturbances accelerate hepatic pathology.

This Collection welcomes original research articles, reviews, and meta-analyses focused on this reciprocal relationship. Given the high prevalence of MASLD in T2D, we especially encourage submissions at the T2D–MASLD–cardiovascular interface. Addressing hepatic and cardiometabolic health in parallel is essential for effective risk reduction and patient care.

This Collection supports and amplifies research related to SDG 3, Good Health and Well-Being.

All submissions in this Collection undergo the journal’s standard peer review process. Similarly, all manuscripts authored by a Guest Editor(s) will be handled by the Editor-in-Chief. As an open access publication, this journal levies an article processing fee (details here). We recognize that many key stakeholders may not have access to such resources and are committed to supporting participation in this issue wherever resources are a barrier. For more information about what support may be available, please visit OA funding and support, or email OAfundingpolicy@springernature.com or the Editor-in-Chief.