From Ions to Inflammation: Immune Cell Transporters as Mediators of Renal and Vascular Dysfunction and Blood Pressure

Immune cells - including macrophages, dendritic cells, T cells, B cells, and NK cells - express a wide variety of ion channels and transporters that govern their activation, metabolism, survival, and migration. By sensing changes in electrolytes, glucose, and other solutes, immune cells modulate the activity of tubular epithelial cells to help restore homeostasis. Through this signalling, immune cells influence sodium handling, vascular tone, and blood pressure regulation within the kidney. Under conditions of metabolic stress, high salt intake, or ischemic injury, dysregulation of these ion channels and transporters can lead to maladaptive inflammatory responses. Pro-inflammatory signals then contribute to vascular and renal injury, further disrupting electrochemical balance and positioning immune cell channels as key instigators of salt-sensitive hypertension.

By redefining the kidney as an electro-immunological hub, this collection aims to deepen our understanding of how ion channels and transporters on immune cells contribute to renal physiology and pathology, with a particular focus on hypertension and both acute and chronic kidney disorders, including (but not limited to) AKI, CKD, DKD, LN, RCC, and FSGS.

To gather new insights in this field, we welcome articles exploring the following:

- Transporter expression profiles in immune cells (e.g., Na⁺, K⁺, Ca²⁺, Cl⁻ channels; NHE; ENaC; Na⁺/K⁺ ATPase; glucose transporters).
- Mechanistic insights into transporter regulation of immune cell activation, antigen presentation, and cytokine release.
- Specific roles of individual channels and transporters in physiology and disease: vascular inflammation, maladaptive repair, salt handling, and blood pressure regulation.
- Glucose transporters and metabolic reprogramming of immune cells in hypertensive kidney disease.
- Crosstalk between immune cell transporters and tubular epithelial transporters in sodium retention and blood pressure elevation.
- Sex differences in immune cell transporter expression and implications for hypertension.
- Targeting immune cell transporters (e.g., ion channel inhibitors, metabolic modulators, nanomedicine approaches).

We welcome submissions of Brief Reports, Case Reports, Conceptual Analyses, Clinical and Preclinical Original Research, Descriptive and Hypothetical Reviews, Systematic Reviews, Mini Reviews, and Opinion Articles.

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
• FAIR² DATA Direct Submission
• General Commentary
• ... View all formats

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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
• FAIR² DATA Direct Submission
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Policy Brief
• Review
• Study Protocol
• Systematic Review
• Technology and Code

Keywords: salt sensitivity, kidney immune cells, ion channels, blood pressure, inflammation, maladaptive, pro-inflammatory, immunology, kidney, renal physiology, pathophysiology, AKI, CDK, DKD, LN, RCC, FSGS, hypertension, acute, cronic, disorders, salt, electrolytes, metabolism, survival, b cell, t cell, nk cell, metabolic modulation, ion channel inhibitos, nanomedicine, tubular epithelia

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.