Evidence map›Paper›PMID 40348345›Full record

ArticleBiochimica et biophysica acta. Molecular cell research2025

Inhibition of NAMPT as a therapeutic strategy to suppress tumor growth in lymphangioleiomyomatosis.

Shahrzad S Fard, Nandini Kundu, Alek S Torres, Christina L Faltas, Julie S Di Martino, Marina K Holz

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochimica et biophysica acta. Molecular cell research, 2025. 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
–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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Shahrzad S FardDepartment of Cell Biology and Anatomy, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America.
Nandini KunduDepartment of Cell Biology and Anatomy, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America.
Alek S TorresDepartment of Cell Biology and Anatomy, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America.
Christina L FaltasDepartment of Cell Biology and Anatomy, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America.
Julie S Di MartinoDepartment of Cell Biology and Anatomy, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America.
Marina K HolzDepartment of Cell Biology and Anatomy, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America; Department of Biochemistry and Molecular Biology, Graduate School of Biomedical Sciences, New York Medical College, Valhalla, New York, United States of America. Electronic address: mholz@nymc.edu.

Funding

Estrogenic signaling upstream and downstream of mTORR35GM128675 · NIGMS · NEW YORK MEDICAL COLLEGE · PI HOLZ, MARINA K · 2018 to 2022
$2.4M
NIGMS NIH HHS R35 GM128675
6 · The paper itself

Abstract

Lymphangioleiomyomatosis (LAM) is a rare, progressive lung disease driven by mutations in the TSC1 or TSC2 genes, leading to constitutive mTORC1 activation and uncontrolled cell proliferation. Current therapies, like rapamycin effectively stabilize disease progression but mainly exert cytostatic effects and promote autophagy, a survival mechanism in LAM cells. These limitations highlight the need for the development of innovative therapies to achieve more effective and lasting results. To explore alternative therapeutic targets, we investigated the role of nicotinamide phosphoribosyltransferase (NAMPT), a key regulator of NAD

Indexed as

AcrylamidesCytokinesLung NeoplasmsLymphangioleiomyomatosisNicotinamide PhosphoribosyltransferasePiperidinesAnimalsAutophagyCell Line, TumorCell ProliferationChick EmbryoHumansMechanistic Target of Rapamycin Complex 1MiceNADSignal TransductionAcrylamidesCytokinesMechanistic Target of Rapamycin Complex 1N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamideNADNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanPiperidinesTSC2 protein, humanTsc2 protein, mouseTuberous Sclerosis Complex 1 ProteinTuberous Sclerosis Complex 2 ProteinTumor Suppressor ProteinsAMP-activated protein kinase (AMPK)AutophagyFK866Lymphangioleiomyomatosis (LAM)Mechanistic target of rapamycin (mTOR)Nicotinamide Phosphoribosyltransferase (NAMPT)Targeted therapyTuberous sclerosis complex (TSC)

Identifiers

PMID40348345
PMCPMC12140862

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.