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NAD⁺ & NMN
Research brief

Mouse, pig and human placental aging linked to macrophage CD38 depleting NAD⁺

In aged placentas from humans, mice and pigs, the abstract reports more macrophage CD38 and less NAD⁺; in experiments, macrophage CD38 depleted NAD⁺ in decidual stromal cells and promoted placental senescence. [1]

Automatic summary · not editorially reviewed

The key findings

  1. Aged placentas in humans, mice and pigs shared increased macrophage CD38 expression and NAD⁺ deficiency. [1]

  2. In experiments, macrophage CD38 depleted NAD⁺ in decidual stromal cells and promoted placental senescence. [1]

  3. NAD⁺ precursors or CD38 inhibitors attenuated age-related placental senescence and rescued intrauterine growth restriction in the reported work. [1]

The source at a glance

Study type / format
Abstract of a preclinical and multi-species laboratory study
Population / context
Placentas from humans, mice and pigs, plus decidual stromal cells and macrophages in experiments.
Summary based on
Study abstract
Original publication
August 27, 2026

Aged placentas in three species show CD38 and NAD⁺ changes

The abstract describes delayed childbearing as increasingly common and calls age-related placental senescence important to understand. Combining metabolomics, single-cell RNA sequencing and spatial transcriptomics, the authors report conserved features of aged placentas in humans, mice and pigs: increased CD38 expression in macrophages and NAD⁺ deficiency. These are described as features of aged placentas, not as causes of aging itself.

Supporting source [1]

Macrophage CD38 depletes stromal-cell NAD⁺ in experiments

Using pharmacological and genetic approaches, the authors report that macrophage CD38 depletes NAD⁺ in decidual stromal cells, thereby promoting placental senescence. They further describe early-onset inflammation and senescence-associated secretory phenotype activity driving CD38 expression in macrophages via the IRF5 pathway. These mechanistic statements come from the abstract; the underlying experiments are not detailed there.

Supporting source [1]

NAD⁺ precursors and CD38 inhibitors in the abstract

The abstract states that treatment with NAD⁺ precursors or CD38 inhibitors attenuated age-related placental senescence, rescued intrauterine growth restriction and improved long-term metabolic outcomes in offspring. It presents CD38 as a potential therapeutic target for age-associated pregnancy complications. These are reported findings and a proposed target, not an established treatment for people; the abstract gives no doses, human trial data or safety results.

Supporting source [1]

How to interpret this

This is an abstract; the full text was not reviewed. It reports no sample sizes, follow-up durations, effect sizes or human trial data, and the treatment results are preclinical findings, not established human benefits.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

[1]
CD38-activated macrophages drive age-related placental senescence by depleting NAD<sup>+</sup> in decidual stromal cells.

Hua L, Yang X, Gao D, Yang X, Jin X, Ma L, Liu W, Li J, Shen Z, Liu L, Wu Y, Yang Y, Zhu C, Li L, Jiang X, Han X, Jin C, Liu G, Feng B, Che L, Xu S, Lin Y, Fang Z, Jin L, Luo T, Zhuo Y, Li M, Wu. · europepmc.org · August 27, 2026

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    conserved features of aged placentas in humans,
  2. Finding 2 ↑

    macrophage CD38 depletes NAD⁺ in decidual stromal
  3. Finding 3 ↑

    treatment with NAD⁺ precursors or CD38 inhibitors

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

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