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.

Cardiovascular Diabetology features a Collection on "Incretin-Based Therapies in Type 2 Diabetes and Obesity: Current Evidence and the Evolving Cardiometabolic Landscape". This is a companion Collection with Cardiovascular Diabetology - Endocrinology Reports with the title "Pleiotropic Actions of Incretin-Based Therapies".

Building upon the growing recognition of cardiometabolic organ protection as a central therapeutic goal, incretin-based therapies have reshaped the management of type 2 diabetes and obesity, extending their clinical relevance far beyond glycemic control. Large-scale cardiovascular outcome trials (CVOTs) have shown that glucagon-like peptide-1 receptor agonists (GLP-1RAs) significantly reduce major adverse cardiovascular events (MACE), redefining cardiometabolic risk management and influencing contemporary therapeutic strategies. Targeting the glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) pathways, these agents enhance glucose-dependent insulin secretion, promote weight reduction, and exert multi-organ effects. Growing evidence supports their impact on vascular function, myocardial metabolism, renal protection, metabolic dysfunction-associated steatotic liver disease (MASLD), and systemic inflammation.

Three principal pharmacological approaches currently characterize incretin-based therapy:

• GLP-1 receptor agonists (GLP-1RAs), mostly injectable medications with proven improved cardiovascular outcomes and weight-reduction.
• Dual GIP/GLP-1 receptor agonists, newer solely injectable medications designed to enhance glycemic control and weight-reduction efficacy.
• DPP-4 inhibitors (also known as gliptins), oral medications which modestly increase endogenous incretin levels and have no impact on cardiovascular outcomes or body weight.

Beyond glucose lowering, incretin-based therapies are increasingly positioned within the broader cardiometabolic framework, with emerging data supporting cardiovascular and renal protection, as well as effects on endothelial function, atherosclerosis, heart failure phenotypes, and chronic kidney disease progression.

Areas of interest include, but are not limited to:

• Classic antidiabetic, anti-obesity and cardioprotective effects
• Cardiovascular outcomes and mechanistic correlates
• Endothelial and vascular biology
• Myocardial metabolism and heart failure subtypes
• Novel renal and hepatoprotective actions
• Optimization and individualized use of existing GLP-1 receptor agonists
• Development of novel GLP-1 receptor agonists and multi-agonist (dual and triple) strategies
• Emerging extra-metabolic actions, including anti-inflammatory and neuroprotective effects
• Combination therapies, including co-formulations with insulin or SGLT2 inhibitors
• Innovative delivery systems, including non-injectable and implantable approaches
• Real-world comparative effectiveness, long-term safety, adherence and treatment durability

This Collection welcomes original research, translational studies, and comprehensive reviews and meta-analyses that provide novel mechanistic insight or clinically relevant evidence to advance understanding of the expanding role of incretin-based therapies in cardiometabolic medicine.

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 journal editorial board. 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.