Despite advancements in glycemic control, cardiovascular disease remains the leading cause of morbidity in diabetes. The plateau in clinical outcomes suggests that we may have overlooked a complex, multi-organ communication network—the vasculome. This Collection seeks to move beyond traditional glucocentric frameworks to better understand endothelial biology as a dynamic interface integrating metabolic, immune, neural, and hormonal signals. We focus on the concept of the endothelial interactome, a heterogeneous and spatially diverse regulatory system that contributes to vascular dysfunction, organ-specific complications, and cardiometabolic risk.

The aim of this Collection is to provide a high-impact platform for research that characterizes site-specific endothelial heterogeneity and its interactions with peripheral organ systems in cardiometabolic disease. We particularly encourage studies that identify molecular and cellular “signatures” (e.g., angiokines, inflammatory mediators, and metabolic regulators) that contribute to organ-specific vascular complications. By integrating systems biology approaches with clinical and translational data, we aim to advance understanding of disease mechanisms and identify novel targets for prevention, risk stratification, and precision therapy, including strategies that address persistent vascular dysfunction despite metabolic control.

We welcome original research articles, clinical investigations, observational cohort studies, randomized clinical trials, high-level reviews, and translational perspectives.

Topics of interest include, but are not limited to:

• Neuro-Immune-Vascular Axis: Interactions between autonomic regulation, immune activation, and vascular inflammation in cardiometabolic disease
• Sex as a Biological Variable: Sex-specific mechanisms contributing to vascular complications in diabetes and metabolic disease
• Epigenetic and Immune Memory: Mechanisms of vascular “trained immunity” and potential strategies for reversal or modulation
• Systems Medicine Approaches: Multi-omics, computational modeling, and organ-on-a-chip platforms to study endothelial heterogeneity and inter-organ communication
• Clinical Translation: Biomarkers, imaging approaches, and therapeutic strategies targeting vascular dysfunction and improving cardiovascular outcomes in diabetes and related metabolic disorders

We invite contributions that bridge basic, translational, and clinical research to advance a more integrated understanding of vascular disease in cardiometabolic disorders. Our goal is to translate mechanistic insights into meaningful clinical outcomes that improve prevention, diagnosis, and treatment in metabolic disease.

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.

Cardiovascular Diabetology features a Collection on "Cardiometabolic and Hepatic Interconnections: From Mechanisms to Clinical Implications". This is a companion Collection with Diabetology & Metabolic Syndrome with the title "MASLD Beyond the Liver: Epidemiology, Pathophysiology, Diagnosis, and Therapeutic Implications in Multisystem Disorders".

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.