Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing 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.
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
22 authors.
Xue-Nan SunTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-2588-6648
Shiuhwei ChenTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Shangang ZhaoTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-9209-8206
Jan-Bernd FunckeTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-2596-3167
Megan VirostekTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0009-0005-4968-2529
Line PedersenTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-1002-4009
Chao LiTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-2060-4835
Chanmin JoungTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-0004-3441
Qian LinTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-6712-7431
Yan LiTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Ayanna CobbTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
May-Yun WangTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Kyounghee MinTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-2546-0236
Lisandro Maya-RamosTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-4424-7537
Giovanna DegasperiTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Junquan LiuTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.ORCID 0000-0002-4348-2180
Zhiqiang AnTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.ORCID 0000-0001-9309-2335
Diana R TomchickDepartment of Biophysics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-7529-4643
R Max WynnTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Da Young OhTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-0687-6479
Philipp E SchererTouchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-0680-3392
Funding
UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeffrey M Zigman · 2022 to 2026
$7.4M
Effects of leptin modulation on health span and lifespanR01AG084646 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Shangang Zhao · 2024 to 2026
$2.0M
Paracrine effects of leptin in regulating visceral fat expansionR01DK138035 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Shangang Zhao · 2024 to 2026
$1.2M
Impact of a Novel Secreted Enzyme J18 on Healthspan and LifespanR00AG068239 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZHAO, SHANGANG · 2023 to 2025
$742k
High-performance slide scanner for multichannel fluorescence, brightfield and polarizationS10OD032267 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI RAMIREZ, DENISE MARIE · 2022 to 2022
Leptin, a hormone primarily secreted by adipocytes, regulates energy balance and systemic metabolism through its interaction with the leptin receptor (LEPR). Beyond these functions, leptin signaling has been implicated in the pathogenesis of tissue fibrosis. Here, we report the x-ray crystal structures of a leptin-neutralizing antibody (hLep3) in the unbound and leptin-bound states. The interaction of this antibody with leptin mimics the interaction of the LEPR with leptin, providing direct insights into the mechanism by which the antibody disrupts leptin signaling. We furthermore evaluate the therapeutic potential of neutralizing leptin with this antibody across distinct mouse models of fibrosis affecting the kidney, liver, lung, heart, and blood vessels. Leptin neutralization markedly inhibited fibrosis progression in all models. Mechanistically, suppression of leptin activity reduces pro-inflammatory and profibrotic processes, underscoring its therapeutic potential. These findings suggest that leptin signaling plays a vital role in tissue fibrosis and that treatment with a leptin-neutralizing antibody may be a promising therapeutic approach.
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.
Leptin as a key driver for organ fibrogenesis. · full record | Socratic