Evidence map›Paper›PMID 34388364›Full record

ArticleStem cell reports2021

Patient-specific iPSC-derived endothelial cells reveal aberrant p38 MAPK signaling in atypical hemolytic uremic syndrome.

Danni Zhou, Ying Tan, Xiaoling Liu, Ling Tang, Hao Wang, Jiaxi Shen, Wei Wang, Lenan Zhuang, Juan Tao, Jun Su and 5 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  3. Review
  4. Hemocyanin controlsVirulence · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
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

15 authors at 9 institutions in 1 country.

Danni ZhouDivision of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; NHC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou 310003, China; Institute of Translational Medicine, Zhejiang University, Hangzhou 310029, China.
Ying TanRenal Division, Department of Medicine, Peking University First Hospital, 8 Xishiku Street, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Ministry of Education of China, Beijing 100034, China.
Xiaoling LiuRenal Division, Department of Medicine, Peking University First Hospital, 8 Xishiku Street, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Ministry of Education of China, Beijing 100034, China.
Ling TangDivision of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; NHC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou 310003, China; Institute of Translational Medicine, Zhejiang University, Hangzhou 310029, China.
Hao WangDepartment of Prenatal Diagnosis (Screening) Center, Hangzhou Women's Hospital (Hangzhou Maternity and Child Health Care Hospital), Hangzhou 310008, China; Department of Cell Biology and Medical Genetics, Zhejiang University School of Medicine, Hangzhou 310058, China.
Jiaxi ShenDivision of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; NHC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou 310003, China; Institute of Translational Medicine, Zhejiang University, Hangzhou 310029, China.
Wei WangDepartment of Cardiology, the Children's Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Lenan ZhuangDepartment of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China.
Juan TaoRenal Division, Department of Medicine, Peking University First Hospital, 8 Xishiku Street, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Ministry of Education of China, Beijing 100034, China.
Jun SuDivision of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; NHC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou 310003, China; Institute of Translational Medicine, Zhejiang University, Hangzhou 310029, China.
Tingyu GongDivision of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China.
Xiaorong LiuDepartment of Nephrology, Beijing Children's Hospital affiliated with Capital Medical University, 56 Nanlishi Road, Beijing 100045, China. Electronic address: lxrbch@sina.com.
Ping LiangDivision of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; NHC Key Laboratory of Combined Multi-organ Transplantation, Hangzhou 310003, China; Institute of Translational Medicine, Zhejiang University, Hangzhou 310029, China. Electronic address: pingliang@zju.edu.cn.
Feng YuRenal Division, Department of Medicine, Peking University First Hospital, 8 Xishiku Street, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Ministry of Education of China, Beijing 100034, China; Department of Nephrology, Peking University International Hospital, Beijing 102206, China. Electronic address: yufengevert1@sina.com.
Minghui ZhaoRenal Division, Department of Medicine, Peking University First Hospital, 8 Xishiku Street, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Ministry of Education of China, Beijing 100034, China; Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100034, China.
First Affiliated Hospital Zhejiang University · CNMinistry of Education of the People's Republic of China · CNPeking University First Hospital · CNZhejiang University · CNBeijing Children’s Hospital · CNBlood Center of Zhejiang Province · CNChildren's Hospital of Zhejiang University · CNHangzhou Women’s Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atypical hemolytic uremic syndrome (aHUS) is a rare disease associated with high morbidity and mortality. Existing evidence suggests that the central pathogenesis to aHUS might be endothelial cell damage. Nevertheless, the role of endothelial cell alterations in aHUS has not been well characterized and the underlying mechanisms remain unclear. Utilizing an induced pluripotent stem cell-derived endothelial cell (iPSC-EC) model, we showed that anti-complement factor H autoantibody-associated aHUS patient-specific iPSC-ECs exhibited an intrinsic defect in endothelial functions. Stimulation using aHUS serums exacerbated endothelial dysfunctions, leading to cell apoptosis in iPSC-ECs. Importantly, we identified p38 as a novel signaling pathway contributing to endothelial dysfunctions in aHUS. These results illustrate that iPSC-ECs can be a reliable model to recapitulate EC pathological features, thus providing a unique platform for gaining mechanistic insights into EC injury in aHUS. Our findings highlight that the p38 MAPK signaling pathway can be a therapeutic target for treatment of aHUS.

Indexed as

MAP Kinase Signaling SystemApoptosisAtypical Hemolytic Uremic SyndromeAutoantibodiesAutoimmunityBiomarkersComplement Factor HDisease SusceptibilityEndothelial CellsEndotheliumHumansInduced Pluripotent Stem Cellsp38 Mitogen-Activated Protein KinasesPhenotypeAutoantibodiesBiomarkersCFH protein, humanComplement Factor Hp38 Mitogen-Activated Protein KinasesaHUSanti-CFH autoantibodiesendothelial dysfunctioniPSC-ECsp38 MAPK

Identifiers

PMID34388364
PMCPMC8452517
OpenAlexW3190200597

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.