Carolina Garcia-de-Alba (She/her)

Hypertension treatment is entering a third era. A new Circulation Research editorial argues that controlling blood pressure, glucose, and cholesterol is no longer enough. The next generation of cardiometabolic therapy should target the biology driving disease—vascular aging, chronic inflammation, and regenerative failure. The review series highlights four major paradigm shifts: • GLP-1 receptor agonists may protect the cardiovascular system by preserving vascular regenerative progenitor cells, suppressing inflammaging, and restoring the balance between vascular injury and repair—not simply through weight loss or glucose lowering. • Mineralocorticoid signaling is increasingly recognized as a central driver of age-related hypertension. Emerging therapies including finerenone, baxdrostat, and lorundrostat could address aldosterone-mediated vascular injury more effectively than conventional approaches. • The RAAS field is evolving beyond ACE inhibitors and ARBs toward RNA therapeutics, tissue-specific targeting, and activation of the protective ACE2–Ang-(1–7)–Mas axis. • Mechanistic GLP-1 biology remains a major frontier, with ongoing efforts to distinguish direct cardiovascular receptor signaling from secondary metabolic effects. The overarching message is that cardiometabolic disease should be viewed as a disorder of vascular resilience, where impaired regeneration, persistent inflammation, and accelerated biological aging become therapeutic targets alongside traditional risk factors. Rather than treating hypertension, obesity, diabetes, and heart failure as separate diseases, future precision medicine may stratify patients according to dominant mechanisms—vascular regenerative cell exhaustion, aldosterone-driven pathology, protective RAAS deficiency, or GLP-1-responsive biology—to deliver mechanism-based therapy instead of one-size-fits-all risk-factor control.