The cardiovascular–kidney–metabolic (CKM) syndrome describes a cluster of interrelated pathophysiological processes involving the cardiovascular system, kidneys, and metabolic pathways. These systems are closely linked through hemodynamic regulation, hormonal signaling, inflammation, and glucose–lipid homeostasis. Dysregulation in any one of these components often triggers maladaptive responses in the others, leading to disease progression across systems.Growing evidence has shown that metabolic disorders such as obesity, insulin resistance, and type 2 diabetes not only contribute to kidney dysfunction but also increase the risk of cardiovascular morbidity and mortality. Metabolic disturbances are also associated with changes in other organs, including skeletal muscle, which may contribute to functional decline and systemic imbalance. Similarly, impaired renal function is known to exacerbate vascular injury and metabolic abnormalities. These interactions are bidirectional and mutually reinforcing, forming the biological foundation of CKM syndrome.Despite the increasing clinical recognition of CKM syndrome, the underlying integrative mechanisms remain poorly understood. Further research is needed to define the molecular, cellular, and systemic drivers of this multisystem network and to identify early indicators of subclinical dysfunction.This Research Topic aims to promote research into the biological, mechanistic, and clinical relevance of CKM syndrome, and to deepen understanding of the interconnected mechanisms underlying this multisystem disease. We invite studies that explore shared pathophysiological pathways, systemic consequences of organ crosstalk, and opportunities for early detection and therapeutic intervention. We welcome studies that examine signaling pathways, inflammatory and metabolic regulators, hemodynamic alterations, and clinical features characterizing this complex network. Submissions that clarify how dysfunction in one organ contributes to pathological changes in others, such as the heart, kidneys, or skeletal muscle, are particularly encouraged. By integrating insights from basic and clinical research, this Topic seeks to advance comprehensive approaches to early diagnosis, risk stratification, and intervention across the CKM continuum.We welcome original research, reviews, translational studies, and mechanistic investigations related to cardiovascular–kidney–metabolic syndrome. Topics may include, but are not limited to:• Interorgan signaling and feedback loops among cardiovascular, renal, and metabolic systems• Roles of inflammation, insulin resistance, and lipid dysregulation in CKM pathogenesis• Mitochondrial function and energy metabolism in CKM-related diseases• Experimental models to study cardiovascular–kidney–metabolic interactions• Structural or functional changes in one organ induced by dysfunction in another, such as effects on the heart, kidneys, or skeletal muscle• Links between CKM dysregulation and clinical conditions such as heart failure, diabetic nephropathy, or metabolic syndrome• Biomarkers or clinical phenotypes indicative of early-stage CKM syndrome• Therapeutic strategies targeting the integrated CKM network
The cardiovascular–kidney–metabolic (CKM) syndrome describes a cluster of interrelated pathophysiological processes involving the cardiovascular system, kidneys, and metabolic pathways. These systems are closely linked through hemodynamic regulation, hormonal signaling, inflammation, and glucose–lipid homeostasis. Dysregulation in any one of these components often triggers maladaptive responses in the others, leading to disease progression across systems.Growing evidence has shown that metabolic disorders such as obesity, insulin resistance, and type 2 diabetes not only contribute to kidney dysfunction but also increase the risk of cardiovascular morbidity and mortality. Metabolic disturbances are also associated with changes in other organs, including skeletal muscle, which may contribute to functional decline and systemic imbalance. Similarly, impaired renal function is known to exacerbate vascular injury and metabolic abnormalities. These interactions are bidirectional and mutually reinforcing, forming the biological foundation of CKM syndrome.Despite the increasing clinical recognition of CKM syndrome, the underlying integrative mechanisms remain poorly understood. Further research is needed to define the molecular, cellular, and systemic drivers of this multisystem network and to identify early indicators of subclinical dysfunction.This Research Topic aims to promote research into the biological, mechanistic, and clinical relevance of CKM syndrome, and to deepen understanding of the interconnected mechanisms underlying this multisystem disease. We invite studies that explore shared pathophysiological pathways, systemic consequences of organ crosstalk, and opportunities for early detection and therapeutic intervention. We welcome studies that examine signaling pathways, inflammatory and metabolic regulators, hemodynamic alterations, and clinical features characterizing this complex network. Submissions that clarify how dysfunction in one organ contributes to pathological changes in others, such as the heart, kidneys, or skeletal muscle, are particularly encouraged. By integrating insights from basic and clinical research, this Topic seeks to advance comprehensive approaches to early diagnosis, risk stratification, and intervention across the CKM continuum.We welcome original research, reviews, translational studies, and mechanistic investigations related to cardiovascular–kidney–metabolic syndrome. Topics may include, but are not limited to:• Interorgan signaling and feedback loops among cardiovascular, renal, and metabolic systems• Roles of inflammation, insulin resistance, and lipid dysregulation in CKM pathogenesis• Mitochondrial function and energy metabolism in CKM-related diseases• Experimental models to study cardiovascular–kidney–metabolic interactions• Structural or functional changes in one organ induced by dysfunction in another, such as effects on the heart, kidneys, or skeletal muscle• Links between CKM dysregulation and clinical conditions such as heart failure, diabetic nephropathy, or metabolic syndrome• Biomarkers or clinical phenotypes indicative of early-stage CKM syndrome• Therapeutic strategies targeting the integrated CKM network