Evidence map›Paper›PMID 40659633›Full record

ReviewCell death discovery2025

CYP51A1 in health and disease: from sterol metabolism to regulated cell death.

Fangquan Chen, RuiRui Liang, Jieting Zhang, Rui Kang, Daolin Tang, Jiao Liu

Abstract readReview
In one paragraph

Review in Cell death discovery, 2025. 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. More than a ring: the emerging role of heme in angiogenesis.Cell communication and signaling : CCS · 2026
    Review
  3. Article
  4. Article
  5. Review
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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

6 authors.

Fangquan ChenDAMP Laboratory, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
RuiRui LiangDAMP Laboratory, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Jieting ZhangThe Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Rui KangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0003-2725-1574
Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA. daolin.tang@utsouthwestern.edu.ORCID http://orcid.org/0000-0002-1903-6180
Jiao LiuDAMP Laboratory, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China. 2018683073@gzhmu.edu.cn.ORCID http://orcid.org/0000-0003-1708-0409

Funding

Guangzhou Municipal Science and Technology Project 2024A03J0895Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2023A1515012496
6 · The paper itself

Abstract

How do cells precisely coordinate sterol metabolism with survival and death signals in diverse physiological and pathological contexts? This fundamental question has gained increasing attention as accumulating evidence reveals that enzymes traditionally associated with lipid biosynthesis may have unexpected regulatory functions beyond metabolism. Cytochrome P450 family 51 subfamily A member 1 (CYP51A1), a conserved sterol 14α-demethylase essential for cholesterol synthesis, exemplifies this emerging concept. Although well-characterized as an antifungal drug target in microorganisms, the roles of human CYP51A1 in development, cell death regulation, and disease pathogenesis remain underexplored. Recent studies have uncovered that CYP51A1 not only contributes to cholesterol homeostasis but also modulates multiple forms of regulated cell death-including apoptosis, ferroptosis, alkaliptosis, and pyroptosis-via sterol intermediates or cholesterol-independent mechanisms. Moreover, dysregulation of CYP51A1 has been implicated in a wide spectrum of diseases, such as cancer, cataracts, Antley-Bixler syndrome, autoimmune disorders, metabolic liver disease and neurodegeneration. In this review, we provide a comprehensive synthesis of CYP51A1's structure, regulatory networks, and non-canonical functions. We propose a unifying framework in which CYP51A1 integrates metabolic reprogramming and cell fate control, highlighting its potential as a therapeutic target across diverse human diseases.

Identifiers

PMID40659633
PMCPMC12260017

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Registered trials

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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.