Evidence map›Paper›PMID 37289024›Full record

ArticleAutophagy2024

Unraveling the Link between Class 1A PI3-Kinase, Autophagy, and Myelodysplasia.

Kristina Ames, Kira Gritsman

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

2 authors at 1 institution in 1 country.

Kristina AmesDepartment of Medical Oncology, Department of Cell Biology, Gottesman Institute of Stem Cell Biology and Regenerative Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.ORCID 0000-0002-6845-0898
Kira GritsmanDepartment of Medical Oncology, Department of Cell Biology, Gottesman Institute of Stem Cell Biology and Regenerative Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.ORCID 0000-0002-1367-1167
Albert Einstein College of Medicine · US

Funding

PI3 Kinase Inactivation in Myelodysplastic SyndromeR01DK130895 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI GRITSMAN, KIRA · 2022 to 2025
$2.2M
PI3K Isoform Dependence in Adult Hematopoiesis and Myeloid LeukemiaR01CA196973 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GRITSMAN, KIRA · 2016 to 2020
$2.0M
Role of the Class IA PI3K in Hematopoietic Stem Cell Self-RenewalF32HL146119 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI AMES, KRISTINA · 2019 to 2022
$213k
PI3 Kinase Inactivation in Myelodysplastic SyndromeR56DK130895 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI GRITSMAN, KIRA · 2021 to 2021
$100k
NCI NIH HHS R01 CA196973NHLBI NIH HHS F32 HL146119NIDDK NIH HHS R01 DK130895NIDDK NIH HHS R56 DK130895
6 · The paper itself

Abstract

Myelodysplastic syndrome (MDS) is a clonal malignancy that develops from hematopoietic stem cells (HSCs), but the underlying mechanisms of MDS initiation are not well understood. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway is often dysregulated in MDS. To investigate how PI3K inactivation affects HSC function, we generated a mouse model in which three Class IA PI3K genes were deleted in hematopoietic cells. Surprisingly, PI3K deficiency caused cytopenias, reduced survival, and multilineage dysplasia with chromosomal abnormalities, consistent with MDS initiation. PI3K-deficient HSCs had impaired autophagy, and pharmacologic treatment with autophagy-inducing reagents improved HSC differentiation. Furthermore, a similar autophagic degradation defect was observed in MDS patient HSCs. Therefore, our study uncovered a crucial protective role for Class IA PI3K in maintaining autophagic flux in HSCs to preserve the balance between self-renewal and differentiation.

Indexed as

AutophagyHematopoietic Stem CellsMyelodysplastic SyndromesAnimalsCell DifferentiationClass I Phosphatidylinositol 3-KinasesHumansMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-Kinasesautophagyhematopoietic stem cellslysosomeMyelodysplastic syndromePI3K/AKTself-renewal

Identifiers

PMID37289024
PMCPMC11062394
OpenAlexW4379768562

What OpenQuestion holds

Textmetadata
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.