Evidence map›Paper›PMID 36601693›Full record

ArticleCell proliferation2023

Activated SOX9+ renal epithelial cells promote kidney repair through secreting factors.

Hao Nie, Zixian Zhao, Dewei Zhou, Dandan Li, Yujia Wang, Yu Ma, Xutao Liu, Wei Zuo

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 13 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Hao NieEast Hospital, School of Medicine, Tongji University, Shanghai, China.
Zixian ZhaoEast Hospital, School of Medicine, Tongji University, Shanghai, China.
Dewei ZhouEast Hospital, School of Medicine, Tongji University, Shanghai, China.
Dandan LiEast Hospital, School of Medicine, Tongji University, Shanghai, China.
Yujia WangEast Hospital, School of Medicine, Tongji University, Shanghai, China.
Yu MaSuper Organ R&D Center, Regend Therapeutics, Shanghai, China.
Xutao LiuSamueli School of Engineering, University of California Los Angeles, Los Angeles, California, USA.
Wei ZuoEast Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0002-4460-0337
Shanghai East Hospital · CNRegend Therapeutics (China) · CNSichuan University · CNUniversity of California, Los Angeles · US

Funding

Guangzhou Medical University annual grantNational Key Research and Development Program of China 2017YFA0104600National Key Research and Development Program of China 2018YFA010880National Natural Science Foundation of China 81770073National Science Fund for Excellent Young Scholars 82122038Shanghai Science and Technology Talents Program 19QB1403100Tongji University (Basic Scientific Research Interdisciplinary Fund and 985 Grant)Youth 1000 Talent Plan of China
6 · The paper itself

Abstract

A broad spectrum of lethal kidney diseases involves the irreversible destruction of the tubular structures, leading to renal function loss. Following injury, a spectrum of tissue-resident epithelial stem/progenitor cells are known to be activated and then differentiate into mature renal cells to replace the damaged renal epithelium. Here, however, we reported an alternative way that tissue-resident cells could be activated to secrete multiple factors to promote organ repair. At single-cell resolution, we showed that the resident SOX9+ renal epithelial cells (RECs) could expand in the acutely injured kidney of both mouse and human. Compared to other cells, the SOX9+ RECs overexpressed much more secretion related genes, whose functions were linked to kidney repair pathways. We also obtained long-term, feeder-free cultured SOX9+ RECs from human urine and analysed their secretory profile at both transcriptional and proteomic levels. Engraftment of cultured human SOX9+ RECs or injection of its conditional medium facilitated the regeneration of renal tubular and glomerular epithelium, probably through stimulating endogenous REC self-activation and mediating crosstalk with other renal cells. We also identified S100A9 as one of the key factors in the SOX9+ REC secretome. Altogether, the abilities to extensively propagate SOX9+ RECs in culture whilst concomitantly maintaining their intrinsic secretory capacity suggest their future application in cell-free therapies and regeneration medicine.

Indexed as

KidneyProteomicsAnimalsEpithelial CellsEpitheliumHumansKidney TubulesMiceSOX9 Transcription FactorSOX9 protein, humanSOX9 Transcription Factor

Identifiers

PMID36601693
PMCPMC10068929
OpenAlexW4313545121

What Socratic holds

Textmetadata
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 Socratic graph.