# Signaling Pathways of the Acquired Immune System and Myocardial Dysfunction in Chronic Kidney Disease—What Do We Know So Far?

## TL;DR

This review explores how immune system signaling contributes to heart problems in chronic kidney disease.

## Contribution

The paper reviews current evidence on how immune cells affect heart changes in CKD.

## Key findings

- T cell subsets show varied associations with heart function in CKD models.
- Tregs may shift to a harmful role in CKD and heart failure.
- B lymphocyte depletion is common in CKD and heart failure but its role in heart damage is unclear.

## Abstract

Aberrant signaling pathways of the acquired immune system are implicated in the development of cardiovascular disease (CVD) and chronic kidney disease (CKD) phenotypes. Understanding the complex abnormalities of lymphocyte subpopulations in CKD is a prerequisite for elucidating their implication in uremic cardiomyopathy. T cell subsets display various patterns of association with indices of myocardial function in both experimental and clinical CKD models. The role of Tregs in CVD and CKD has attracted significant research interest. Although experimental data suggest a protective role of Tregs from the development of arterial hypertension- and pressure overload-induced myocardial hypertrophy, there might be a change in the regulatory T cell (Treg) phenotype towards a profibrotic one in the settings of CKD and heart failure. Depletion of B lymphocytes is a hallmark of CKD and heart failure, bearing adverse prognostic significance, yet evidence of B lymphocytes’ involvement in the pathogenesis of myocardial damage is currently lacking. Considering that myocardial remodeling is the final outcome of diverse pathogenic processes targeting the heart, the aim of this review is to present the evidence available up to now regarding the role of acquired immune cells in the pathogenesis of the structural and functional alterations of the myocardium in CKD.