The Immune Transportome: Ion Channels and Transporters in Cardiorenal Disease

Cardiorenal disease is shaped by inflammation, vascular dysfunction, altered sodium handling, and progressive tissue injury. Yet the mechanisms linking these processes remain incompletely defined. One underexplored layer is the set of ion channels and solute transporters that control immune-cell behaviour.

Immune cells sense salt, glucose, pH, oxygen tension, tissue damage, and mechanical stress through ion flux, membrane potential, osmotic balance, substrate transport, and calcium signalling. These processes influence immune-cell activation, migration, cytokine release, inflammasome formation, metabolic state, and survival.

This is highly relevant to salt-sensitive hypertension, AKI, CKD, diabetic kidney disease, lupus nephritis, FSGS, IgA nephropathy, cardiorenal syndrome, preeclampsia, and vascular inflammation. These conditions share maladaptive immune activation, altered transport, and renal or vascular injury, but the links between these layers remain poorly integrated.

Redefining the kidney as an electro-immunological hub, the aim of this Research Topic is to the characterize the immune transportome mapping how immune-cell ion channels and transporters contribute to renal inflammation, vascular dysfunction, sodium handling, blood-pressure regulation, sex differences, and therapeutic response. By connecting physiology, immunology, and pharmacology, the goal is to move beyond descriptive inflammation and identify immune-transport pathways that can explain disease progression, guide biomarkers, and open new routes for intervention.

To achieve this aim, the Research Topic welcomes articles addressing the following areas:

1. Immune-cell ion channels and transporters
We welcome studies on immune-cell expression, regulation, and function of ENaC, NHE, Na⁺/K⁺-ATPase, SGLT2, GLUTs, NCC, NKCC, Kv1.3, KCa3.1, P2X7, TRP channels, Piezo channels, ClC channels, TMEM16A, ORAI/STIM, CRAC channels, and related transport pathways.

2. Immune activation and inflammatory signalling
We welcome work on macrophage polarisation, dendritic-cell activation, antigen presentation, cytokine release, inflammasome activation, Th17/Treg balance, CD8⁺ T cells, neutrophils, B cells, NK cells, oxidative stress, isolevuglandins, purinergic signalling, and immune-cell migration.

3. Renal, vascular, and cardiorenal disease
We welcome studies that link immune-transporter biology to salt-sensitive hypertension, resistant hypertension, AKI, CKD, diabetic kidney disease, lupus nephritis, FSGS, IgA nephropathy, renal fibrosis, hypertensive kidney disease, cardiorenal syndrome, endothelial dysfunction, vascular inflammation, and preeclampsia.

4. Tissue crosstalk
We welcome studies on tubular-immune, endothelial-immune, podocyte-immune, perivascular-immune, and fibroblast-immune crosstalk. This includes work on tubular epithelial injury, podocyte stress, endothelial activation, perivascular inflammation, fibrosis, maladaptive repair, and sodium retention.

5. Sex differences
We especially encourage studies on sex-specific immune-cell transporter expression, sex-biased salt sensitivity, sex differences in renal inflammation and vascular dysfunction, pregnancy, preeclampsia, menopause, sex hormones, autoimmune kidney disease, and sex-specific drug response.

6. Clinical and translational studies
We welcome human immune-cell studies, PBMC analyses, monocyte and macrophage studies, kidney biopsy analyses, urinary extracellular vesicles, biomarker studies, patient cohorts, human salt-sensitivity studies, clinical trial sub-analyses, and drug-response studies.

7. Omics, models, and methods
We welcome single-cell RNA sequencing, spatial transcriptomics, proteomics, phosphoproteomics, metabolomics, systems biology, organoids, tubuloids, organ-on-chip models, ex vivo systems, animal models, and computational approaches that connect transporter biology to immune function.

8. Therapeutic targeting and pharmacology
We welcome work on SGLT2 inhibitors, mineralocorticoid receptor antagonists, ENaC modulators, NHE inhibitors, P2X7 antagonists, NLRP3 inhibitors, Kv1.3 blockers, KCa3.1 blockers, TRP and Piezo modulators, ClC and TMEM16A modulators, ORAI/STIM inhibitors, nanomedicine, targeted delivery, and drug repurposing.

Journal Fit
Because this Research Topic brings together physiology, immunology, and pharmacology, it is suited to a broad contributor community.


* Physiology-focused contributions may address renal transport, sodium handling, blood pressure, vascular function, tissue crosstalk, and sex differences in organ physiology.

* Immunology-focused contributions may address macrophages, dendritic cells, T cells, B cells, neutrophils, NK cells, NLRP3, inflammasomes, antigen presentation, cytokines, Th17/Tregs, and immune-cell metabolism.

* Pharmacology-focused contributions may address druggable transporters, ion-channel inhibitors, SGLT2 inhibitors, MR antagonists, P2X7/NLRP3 inhibitors, Kv1.3 and KCa3.1 blockers, TRP/Piezo modulators, ORAI/STIM inhibitors, targeted delivery, and drug repurposing.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Classification
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Classification
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Policy Brief
• Review
• Study Protocol
• Systematic Review
• Technology and Code

Keywords: ion channels, immune transportome, solute transporters, cardiorenal syndrome, salt-sensitive hypertension, electro-immunology, vascular inflammation, macrophage polarization, renal pharmacology, sex differences, SGLT2 inhibitors, mineralocorticoid receptor antagonists, epithelial-immune crosstalk, NLRP3 inflammasome, purinergic signaling, vesicles, vesicles calcium signaling, preeclampsia, renal fibrosis, PBMCs, single-cell RNA-seq, TRP channels, Piezo channels, Kv1.3 potassium channel, KCa3.1 channel, ENaC NHE1 sodium handling

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.