Evidence map›Paper›PMID 41882522›Full record

ArticleBMC molecular and cell biology2026

Investigating the roles of macrophage age and circulating extracellular vesicles in cytoprotection of hypoxic renal tubular cell stress.

Dora Livkisa, David J Lundy, Tsung-Lin Lee, Barbara Szomolay, Chia-Te Liao

Abstract read
In one paragraph

Article in BMC molecular and cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Dora Livkisa *International PhD Program in Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, New Taipei City, 235603, Taiwan.
David J Lundy *International PhD Program in Biomedical Engineering, Taipei Medical University, 301 Yuantong Road, New Taipei City, 235603, Taiwan.
Tsung-Lin LeeDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, 235603, Taiwan.
Barbara SzomolaySystems Immunity Research Institute, Cardiff University School of Medicine, Cardiff, UK.
Chia-Te LiaoDivision of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, 235603, Taiwan. ctliao19386@tmu.edu.tw.

Funding

Taipei Medical University-Shuang Ho Hospital, Ministry of Health and Welfare 111TMU-SHH-19, 113TMU-SHH-26
6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) involves complex crosstalk between tubular epithelial cells (TECs) and immune cells. Extracellular vesicles (EVs) and ageing have emerged as modulators of this process.

methodsWe investigated the effects of circulating plasma EVs from young (Y_EVs) and old (O_EVs) mice on hypoxic TEC stress, using bone marrow–derived macrophages (BMDMs) from young or old mice, which were pre-conditioned with EVs. First, direct effects of EVs on TEC viability were assessed following hypoxia/reoxygenation injury. We then examined macrophage responses to hypoxic TEC secretomes with or without EV priming, and tested whether EV-primed BMDM secretomes modulated TEC damage, in terms of viability, cytokine expression, and epithelial–mesenchymal transition (EMT).

resultsEVs exerted no direct protective effect on hypoxic TECs, and no significant differences were observed between Y_EVs and O_EVs in any condition. Instead, macrophage donor age was the most significant determinant of outcomes. Conditioned medium from old BMDMs consistently improved TEC viability compared to young BMDMs. In agreement with this, the old mouse BMDM secretome also suppressed hypoxia-induced cytokine expression (Il6, Ccl2) and EMT marker induction (Acta2, Fn1) in hypoxic TECs. EV pre-treatment of BMDMs did not significantly alter these effects in either macrophage group. Thus, BMDM donor age, rather than EV donor age, was the critical driver of cytoprotection and inflammatory modulation in this model.

conclusionCirculating plasma EV age had no significant direct or indirect impacts on TEC viability, inflammatory responses or EMT processes under the tested conditions. This contrasts with prior studies which have suggested broadly rejuvenating effects of young EVs and detrimental effects of old EVs. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

CytoprotectionExtracellular VesiclesKidney TubulesMacrophagesAcute Kidney InjuryAgingAnimalsCell HypoxiaCell SurvivalCulture Media, ConditionedCytokinesEpithelial CellsEpithelial-Mesenchymal TransitionMaleMiceMice, Inbred C57BLCulture Media, ConditionedCytokinesAgeingExtracellular vesicleKidney tubular cell stressMacrophage

Identifiers

PMID41882522
PMCPMC13141442

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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.