Key result
Immune cell activation drives cardiorenal inflammation and end-organ damage across key hypertensive signaling pathways.
Why the study?
In hypertension, renal and cardiovascular dysfunctions form a self-perpetuating feedback loop coordinated by immune cells. This narrative review examines the mechanisms by which immune cells integrate signals from high salt, the RAAS, and the SNS to drive chronic inflammation and end-organ damage, alongside counter-regulatory pathways and emerging immunomodulatory therapeutic strategies.
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This narrative review synthesizes the mechanisms by which immune cells integrate signals from high salt, the renin-angiotensin-aldosterone system, and the sympathetic nervous system to coordinate cardiorenal crosstalk and drive end-organ damage in hypertension, highlighting emerging immunomodulatory therapeutic targets.
Hypertension remains the leading preventable cause of cardiovascular disease and premature death worldwide. In the hypertensive state, renal and cardiovascular dysfunctions become entrenched in a self-perpetuating feedback loop, with immune cells emerging as central coordinators of this pathological crosstalk. This review examines the mechanisms by which immune cells integrate signals from high salt, the renin-angiotensin-aldosterone system (RAAS), and the sympathetic nervous system (SNS) to drive chronic inflammation and end-organ damage. We highlight the salt-dendritic cell-isolevuglandin (IsoLG)-T cell axis as a critical pathway linking dietary sodium to immune activation and hypertension. We also explore bidirectional interactions between immune cells and RAAS components, as well as neuro-immune crosstalk that amplifies sympathetic outflow. Counter-regulatory mechanisms, including the ACE2/Ang-(1-7)/Mas axis, the kallikrein-kinin system, Urodilatin, Klotho, and renalase, provide endogenous braking signals that limit inflammation. Finally, we discuss emerging immunomodulatory therapeutic strategies and identify key unanswered questions for future research. Understanding immune cells as central coordinators of cardiorenal communication offers new opportunities for precision medicine approaches to hypertension.
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Wang et al. (2026) conducted a review in Hypertension. Immune cells and immunomodulatory therapeutic strategies was evaluated. Immune cells integrate high salt, RAAS, and sympathetic signals to drive cardiorenal inflammation and end-organ damage in hypertension, offering targets for immunomodulatory therapy.
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