Evidence map›Paper›PMID 40738832›Full record

ReviewTrends in cell biology2026

Lessons in longevity from blood stem cells under protein stress.

André Catic

Abstract readReview
In one paragraph

Review in Trends in 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.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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

1 author.

André CaticDepartment of Molecular and Cellular Biology, Huffington Center on Aging, Stem Cells and Regenerative Medicine Center, Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA. Electronic address: Catic@bcm.edu.

Funding

Structural Proteome Diversity as a Determinant of Hematopoietic AgingR56DK141457 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CATIC, ANDRE, DI STEFANO, BRUNO · 2025 to 2025
$200k
NIDDK NIH HHS R56 DK141457
6 · The paper itself

Abstract

Blood stem cells are among the body's longest-living cells despite being highly vulnerable to proteotoxic damage, which accelerates their aging. To maintain protein homeostasis (proteostasis), hematopoietic stem cells (HSCs) employ mechanisms such as reduced translation rates, high chaperone activity, autophagy, and selective protein degradation. These strategies mitigate protein misfolding, maintain quiescence, and preserve regenerative potential. Disruptions in proteostasis can lead to the elimination of impaired HSCs through differentiation or apoptosis, ensuring the integrity of the stem cell pool. Due to the systemic impact of the blood on aging and its experimental and clinical accessibility, investigating HSC proteostasis provides insights into longevity and potential therapeutic strategies. This review examines emerging mechanistic links between proteostasis and HSC fate, concluding with unresolved questions and challenges of the current research.

Indexed as

Hematopoietic Stem CellsLongevityProteostasisStress, PhysiologicalAnimalsAutophagyHumansagingautophagyhematopoietic stem cells (HSCs)proteasomeprotein homeostasis (proteostasis)translation control

Identifiers

PMID40738832
PMCPMC12453298

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.