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.

The rising prevalence of obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD)—a condition characterized by hepatic steatosis and metabolic impairment—along with their cardiovascular complications, underscores the urgent need to promote physical activity. Exercise triggers the release of exerkines — a diverse group of signaling molecules including cytokines, lipids, nucleic acids, peptides, and metabolites — that act via endocrine, paracrine, and autocrine mechanisms. Many exerkines are packaged into extracellular vesicles, enabling their transport and communication between distant tissues. These signals mediate local and systemic adaptations with potential therapeutic implications.

While initial studies focused on myokines, it is now clear that organs such as the liver, adipose tissue, heart, and skeletal muscle also contribute to the exerkine network. Advances in multi-omics and systems biology are revealing how these exercise-induced signals modulate key metabolic and inflammatory pathways across tissues. These insights are shedding new light on the pathophysiology of diabetes and cardiovascular disease and may inform the development of personalized interventions to prevent or treat cardiometabolic disorders. This new Collection welcomes submissions in, but not limited to, the following areas:

- The metabolic and molecular effects of acute and chronic exercise in humans and animal models.

- Exerkine-mediated signal transduction pathways (e.g., AMPK, mTOR, PGC-1α).

- Multi-omics profiling of exercise responses (e.g., metabolomics, transcriptomics, epigenomics).

- Sex, modality, intensity, and duration as modulators of exerkine release and action.

- Translational potential of exerkines in treating diabetes and the Cardiovascular-Kidney-Metabolic (CKM) syndrome.

This Collection welcomes original research articles, meta-analyses, and review articles. Submissions using preclinical, translational, or clinical approaches are all considered.

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.