Vascular-Immune Interactions in Cardiovascular Aging: Novel Mechanisms and Biomarkers

About this Research Topic

Submission deadlines

  1. Manuscript Summary Submission Deadline 31 May 2026 | Manuscript Submission Deadline 30 November 2026

  2. This Research Topic is currently accepting articles.

Background

Cardiovascular aging is increasingly recognized as the result of a dynamic interplay between the vascular and immune systems rather than passive “wear and tear.” With advancing age, endothelial cells lose their capacity to maintain vascular tone, barrier integrity, and antithrombotic function, while smooth muscle cells and the extracellular matrix remodel in ways that promote stiffness and impaired tissue perfusion. In parallel, the immune system drifts toward chronic, low‑grade inflammation (“inflammaging”), marked by dysregulated innate and adaptive responses, immune cell senescence, and altered cytokine and chemokine networks. This state fuels endothelial activation, oxidative stress, and maladaptive repair, thereby accelerating atherosclerosis, microvascular dysfunction, heart failure, and other age‑related cardiovascular syndromes. Emerging evidence implicates clonal hematopoiesis, trained immunity, and shifts in myeloid and lymphoid cell populations as direct modulators of vascular phenotype in aging. However, the underlying mechanisms and the identification of robust, clinically useful biomarkers that capture this vascular–immune axis remain incomplete.

This Research Topic aims to elucidate how vascular–immune crosstalk drives cardiovascular aging and to highlight novel biomarkers and therapeutic entry points along this axis. We welcome original research, reviews, mini‑reviews, and perspectives spanning basic, translational, and clinical science.

This collection welcomes contributions in the following areas, among others:

Cellular and molecular pathways governing vascular–immune interactions in aging (e.g., endothelial activation, senescence, clonal hematopoiesis, trained immunity).

Contributions of specific immune cell subsets (macrophages, T cells, B cells, NK cells, neutrophils, innate lymphoid cells) to vascular aging, arterial stiffness, and microvascular rarefaction.

Novel circulating and tissue biomarkers (proteomic, transcriptomic, metabolomic, epigenetic, extracellular vesicle‑based) that reflect vascular–immune dysregulation in older individuals.

Imaging and functional biomarkers (e.g., vascular ultrasound, PET/MRI, flow‑mediated dilation, pulse wave velocity) integrated with immune and inflammatory signatures.

Sex, metabolic, and environmental modifiers (e.g., obesity, diabetes, pollution, diet, physical activity) shaping vascular–immune interactions across the lifespan.

Translational and interventional studies targeting vascular–immune pathways (pharmacologic, biologic, lifestyle, or geroscience‑guided strategies) to prevent, delay, or reverse cardiovascular aging.

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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
  • Clinical Trial
  • Data Report
  • Editorial
  • FAIR² Data
  • General Commentary
  • Hypothesis and Theory
  • Methods

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

Keywords: Cardiovascular aging, Vascular–immune crosstalk, Inflammaging, Endothelial dysfunction, Biomarkers

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.

Topic editors

Manuscripts can be submitted to this Research Topic via the main journal or any other participating journal.