NAD+ · research summary

Integrated Metabolomic and Bioenergetic Profiling Reveals Axl as a Key Regulator of Macrophage Homeostasis.

European journal of immunology · 2026. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

In vivo and in vitro study using Axl-deficient mice and peritoneal macrophages
“Here, we combined phenotypic, functional, metabolomic, and bioenergetic analyses to define how Axl deficiency alters peritoneal macrophages (PMs) under steady‐state conditions.”

Subjects

Peritoneal macrophages from wild-type and Axl-deficient mice
“full‐body (global) Axl−/− mice exhibited a significant reduction in PMs compared with WT controls”

Sample size

Variable sample sizes per experiment, ranging from n=5 to n=10
“Data are presented as mean ± SD from one experiment (WT, n = 7; Axl−/−, n = 8).”

Duration

Mice aged 8 to 12 weeks; in vitro assays conducted for up to 48 hours
“Male and female C57BL/6 wild‐type (WT) and Axl−/− mice, aged 8 to 12 weeks, were generously provided by Dr. Brian Kelsall”

Reported findings

Axl deficiency reduces peritoneal macrophage numbers and shifts phenotype toward a less mature, monocyte-like state
“Axl− / − PMs exhibited reduced cell numbers, downregulation of resident macrophage markers, and increased Ly6C expression, indicating a shift toward a less mature, monocyte‐like phenotype.”
Axl deficiency disrupts central carbon metabolism, including glycolysis and TCA cycle intermediates
“Metabolomic profiling revealed broad disruption of central carbon metabolism, including reduced glycolytic intermediates, depletion of tricarboxylic acid (TCA) cycle metabolites, and decreased NAD+/NADH and NADP+/NADPH pools.”
Axl deficiency impairs mitochondrial respiration and antioxidant defenses, extending to systemic liver dysfunction
“Bioenergetic assessment demonstrated pronounced mitochondrial dysfunction, characterized by reduced maximal respiration, elevated proton leak, and limited oxidative phosphorylation flexibility.”

Source: PubMed 42847323 · DOI 10.1002/eji.70293 · all study summaries

Reported findings

Axl deficiency reduces peritoneal macrophage numbers and shifts phenotype toward a less mature, monocyte-like state

“Axl− / − PMs exhibited reduced cell numbers, downregulation of resident macrophage markers, and increased Ly6C expression, indicating a shift toward a less mature, monocyte‐like phenotype.”

Axl deficiency disrupts central carbon metabolism, including glycolysis and TCA cycle intermediates

“Metabolomic profiling revealed broad disruption of central carbon metabolism, including reduced glycolytic intermediates, depletion of tricarboxylic acid (TCA) cycle metabolites, and decreased NAD+/NADH and NADP+/NADPH pools.”

Axl deficiency impairs mitochondrial respiration and antioxidant defenses, extending to systemic liver dysfunction

“Bioenergetic assessment demonstrated pronounced mitochondrial dysfunction, characterized by reduced maximal respiration, elevated proton leak, and limited oxidative phosphorylation flexibility.”