Evidence map›Paper›PMID 41237921›Full record

ArticleMolecules and cells2025

Deficient chaperone-mediated autophagy in macrophages aggravates colitis and colitis-associated tumorigenesis in mice.

Weichun Zhu, Zehao Chen, Yunqian Gao, Chungang Zhai, Xia Li, Ning Wang, Kang Fu, Wentao Chen, Jieqiong Peng, Dan Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecules and cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. 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

12 authors.

Weichun ZhuState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: 202120808@mail.sdu.edu.cn.
Zehao ChenState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: 2023230002@mail.sdu.edu.cn.
Yunqian GaoState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: gaoyunqian@mail.sdu.edu.cn.
Chungang ZhaiState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: zhaichungang87@sdu.edu.cn.
Xia LiDepartment of Gastroenterology, Shandong Second Provincial General Hospital, Jinan, Shandong, China. Electronic address: 895532751@qq.com.
Ning WangState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: 202115560@mail.sdu.edu.cn.
Kang FuState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: 201935354@mail.sdu.edu.cn.
Wentao ChenState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: 202035711@mail.sdu.edu.cn.
Jieqiong PengDepartment of Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China. Electronic address: 15589116608@163.com.
Dan XuState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of General Practice, Qilu Hospital of Shandong University, Jinan, China. Electronic address: 202289325907@sdu.edu.cn.
Lei QiaoState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: qiaolei@sdu.edu.cn.
Wenqiang ChenState Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012. Electronic address: 199262000802@sdu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chaperone-mediated autophagy (CMA) is a highly selective form of autophagy responsible for the degradation of specific cytosolic proteins within lysosomes. Recent research has established a significant correlation between CMA and colorectal cancer (CRC). However, the majority of current research focuses on tumor parenchymal cells, with limited attention paid to the expression and role of CMA in tumor stromal cells, particularly in tumor-associated macrophages (TAMs). In this study, we generated myeloid-specific LAMP2A-knockout and knock-in mice to investigate the role of macrophage CMA in dextran sodium sulfate (DSS)-induced colitis and azoxymethane/dextran sodium sulfate-induced CRC. Our findings indicated that the expression of LAMP2A, the rate-limiting component of CMA, was reduced in tumor-associated macrophages of both human and mouse CRC tissues. The knockout of LAMP2A in macrophages exacerbated experimentally induced colitis and colitis-related CRC, whereas its overexpression in macrophages alleviated the progression of colitis and CRC in mice. Notably, we observed increased angiogenesis within the tumor mass of CRC tissues from LAMP2A-mØKO mice. Mechanistically, LAMP2A deficiency elevated the protein levels of HIF-1α, thereby enhancing the secretion of its target genes, vascular endothelial growth factor A and IL-1β, which are 2 important proangiogenic cytokines. Our study suggests that the activation of CMA in macrophages may represent a promising therapeutic strategy for the treatment of CRC.

Indexed as

CarcinogenesisChaperone-Mediated AutophagyColitisColorectal NeoplasmsLysosomal-Associated Membrane Protein 2MacrophagesAnimalsDextran SulfateHumansMiceMice, Inbred C57BLMice, KnockoutDextran SulfateLysosomal-Associated Membrane Protein 2AngiogenesisChaperone-mediated autophagyColorectal cancerHypoxia-inducible factor 1 alphaTumor-associated macrophages

Identifiers

PMID41237921
PMCPMC12712685

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.