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bioRxiv

Age linked to shifts in heart immune-cell gene activity in mice

An experiment in young and aged mice found both higher and lower activity in gene programs in heart immune cells 24 hours after an inflammatory challenge.

Paper by Q. Yu, H. Gao, F. Fang, J. Du, M. Wang · Department of Surgery, Center for Surgical Sciences, Indiana University School of Medicine
Heart sections beside laboratory mice show immune cells and dark blue-green mitochondria on one side, larger immune cells and gray mitochondria on the other.
Preprint: experiments in young and aged C57BL/6 mice, 24 h, against young mice receiving LPSMechanisms

The catch: More severe illness in aged mice could explain their different gene activity

Edited by Boris Djordjevic · AgingResearch.News

Paper
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An experiment in young and aged C57BL/6 mice examined how age related to gene activity in immune cells in heart tissue outside blood vessels during systemic inflammation. Researchers injected lipopolysaccharide, a bacterial molecule that triggers inflammation, at 5 milligrams per kilogram of body weight, or a control solution. They collected heart immune cells 24 hours later and measured gene activity in individual cells.

After the inflammatory challenge, aging was associated with both increases and decreases in gene programs—groups of genes involved in related tasks. Four immune-cell populations shared reduced representation of programs related to mitochondria, the cells’ energy-producing structures. Two populations of macrophages, cells that engulf microbes and debris, showed increases in programs associated with tissue remodeling and repair. Aged mice experienced more severe illness.

Why it matters

Sepsis disproportionately affects older adults and often involves heart dysfunction. Understanding the heart’s immune response is relevant to how aging shapes vulnerability to this illness.

Caveats

Changes in gene activity do not establish changes in energy production or tissue repair. This mouse study is a preprint, not yet peer-reviewed, and does not establish what happens in human sepsis.

Where the evidence stands

Inflammation

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 1,019 independent labs in 75 countries
  • 194 findings against
  • Funders: National Institutes of Health and others
  • 365 of 4,393 findings with company ties

Cell killing (cytotoxicity)

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 58 independent labs in 20 countries
  • 1 finding against
  • Funders: National Institutes of Health and others
  • 12 of 67 findings with company ties

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The paper

Aging reshapes cardiac extravascular leukocyte transcription through bidirectional remodeling during LPS-induced endotoxemia

Q. Yu, H. Gao, F. Fang, J. Du, M. Wang

Department of Surgery, Center for Surgical Sciences, Indiana University School of Medicine

bioRxiv, Nov 3, 2026, Open access, CC BY-NC, Preprint, not yet peer-reviewed

doi.org/10.64898/2026.11.02.763785

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