Evidence map›Paper›PMID 39887553›Full record

ArticleAging cell2025

CAV1 Exacerbates Renal Tubular Epithelial Cell Senescence by Suppressing CaMKK2/AMPK-Mediated Autophagy.

Liya Sun, Lujun Xu, Tongyue Duan, Yiyun Xi, Zebin Deng, Shilu Luo, Chongbin Liu, Chen Yang, Huafeng Liu, Lin Sun

Abstract read
In one paragraph

Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Aging Disrupts L-type CaCirculation research · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. 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

10 authors.

Liya SunDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Lujun XuDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Tongyue DuanDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Yiyun XiDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Zebin DengDepartment of Urology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Shilu LuoDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Chongbin LiuDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Chen YangGuangdong Provincial Key Laboratory of Autophagy and Major Chronic non-Communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Huafeng LiuGuangdong Provincial Key Laboratory of Autophagy and Major Chronic non-Communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Lin SunDepartment of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID 0000-0002-4544-0822

Funding

National Natural Science Foundation of China 81730018National Natural Science Foundation of China 82370730
6 · The paper itself

Abstract

Renal proximal tubular epithelial cell (PTEC) senescence and defective autophagy contribute to kidney aging, but the mechanisms remain unclear. Caveolin-1 (CAV1), a crucial component of cell membrane caveolae, regulates autophagy and is associated with cellular senescence. However, its specific role in kidney aging is poorly understood. In this study, we generated Cav1 gene knockout mice and induced kidney aging using D-galactose (D-gal). The results showed that CAV1 expression increased in the renal cortex of the aging mice, which was accompanied by exacerbated renal interstitial fibrosis, elevated levels of senescence-associated proteins γH2AX and p16

Indexed as

AMP-Activated Protein KinasesAutophagyCalcium-Calmodulin-Dependent Protein Kinase KinaseCaveolin 1Cellular SenescenceEpithelial CellsKidney TubulesAnimalsHumansKidney Tubules, ProximalMaleMiceMice, KnockoutPhosphorylationAMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase KinaseCAMKK2 protein, humanCamkk2 protein, mouseCav1 protein, mouseCaveolin 1AMPKAutophagyCaMKK2CAV1Kidney AgingRenal Tubular Epithelial Cell

Identifiers

PMID39887553
PMCPMC12073896

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.