Evidence map›Paper›PMID 36846656›Full record

ReviewHeliyon2023

Is the proximal tubule the focus of tubulointerstitial fibrosis?

Zhi Peng, Hui Wang, Jiaoyun Zheng, Jie Wang, Yang Xiang, Chi Liu, Ming Ji, Huijun Liu, Lang Pan, Xiaoqun Qin and 1 more

Abstract readReview
In one paragraph

Review in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Targeting renal tubular epithelial cellsActa pharmaceutica Sinica. B · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Claudin-2 Mediates the Proximal Tubular Epithelial Cell-Fibroblast Crosstalk via Paracrine CTGF.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    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

11 authors.

Zhi PengDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Hui WangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Jiaoyun ZhengDepartment of Pathology, The Second Xiangya Hospital, Central South University, Changsha, China.
Jie WangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Yang XiangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Chi LiuDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Ming JiDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Huijun LiuDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Lang PanDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Xiaoqun QinDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Xiangping QuDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulointerstitial fibrosis (TIF), a common end result of almost all progressive chronic kidney diseases (CKD), is also the best predictor of kidney survival. Almost all cells in the kidney are involved in the progression of TIF. Myofibroblasts, the primary producers of extracellular matrix, have previously received a great deal of attention; however, a large body of emerging evidence reveals that proximal tubule (PT) plays a central role in TIF progression. In response to injury, renal tubular epithelial cells (TECs) transform into inflammatory and fibroblastic cells, producing various bioactive molecules that drive interstitial inflammation and fibrosis. Here we reviewed the increasing evidence for the key role of the PT in promoting TIF in tubulointerstitial and glomerular injury and discussed the therapeutic targets and carrier systems involving the PT that holds particular promise for treating patients with fibrotic nephropathy.

Indexed as

Chronic kidney diseaseExtracellular matrixProximal tubuleTubulointerstitial fibrosis

Identifiers

PMID36846656
PMCPMC9950842

What OpenQuestion holds

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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.