ReviewBiomolecules2026
IL-15 Signaling Pathways in the Kidney: Established Mechanisms and Hypotheses for Exercise-Associated Stress.
Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Interleukin-15 (IL-15) is an immunoregulatory cytokine also recognized as a myokine, with experimentally demonstrated cytoprotective and metabolic effects. Renal tubular epithelial cells (TECs) and podocytes express components of the IL-15 receptor system, but the role of IL-15 in exercise-associated renal adaptation remains unclear. This review distinguishes evidence from renal experimental models from hypotheses regarding exercise-induced renoprotection. Cell-culture and preclinical studies support a role for IL-15 in promoting TEC survival and attenuating profibrotic responses. Separate studies in podocytes demonstrate a functional role for STAT5 in autophagy regulation and improvements in mitochondrial fusion and respiration in response to IL-15, with optic atrophy 1 (OPA1) implicated in the latter response. These findings do not establish a single integrated pathway or demonstrate that the same protective mechanisms operate during exercise. Strenuous exercise may transiently increase tubular stress- or injury-associated biomarkers; however, these increases do not necessarily indicate clinically significant acute kidney injury (AKI) and should be interpreted alongside measures of renal function and the clinical context. We outline a conceptual framework that distinguishes potentially protective responses in renal parenchymal cells from IL-15-dependent immune activation that may contribute to injury in selected disease settings. Cytokine availability, exposure duration, mode of presentation, receptor composition, and inflammatory context may influence these outcomes, but their roles in renal responses to exercise remain to be established. An increase in circulating IL-15 alone does not establish its skeletal muscle origin, delivery to the kidney, or biological activity in renal target cells. The key unresolved question is whether IL-15 produced by skeletal muscle in response to exercise reaches renal target cells in a biologically active form and confers measurable renoprotection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.