Evidence map›Paper›PMID 27048819›Full record

ReviewCellular and molecular life sciences : CMLS2016

Regulation of necrotic cell death: p53, PARP1 and cyclophilin D-overlapping pathways of regulated necrosis?

Yuan Ying, Babu J Padanilam

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 112 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
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  15. Article
  16. Orexins in apoptosis: a dual regulatory role.Frontiers in cellular neuroscience · 2024
    Review
  17. Review
  18. Article
  19. Review
  20. Article

7 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Yuan YingDepartment of Cellular and Integrative Physiology, 985850 University of Nebraska Medical Center, Omaha, NE, 68198-5850, USA.
Babu J PadanilamDepartment of Cellular and Integrative Physiology, 985850 University of Nebraska Medical Center, Omaha, NE, 68198-5850, USA. bpadanilam@unmc.edu.
University of Nebraska Medical Center · US

Funding

Regulation of Apoptosis in Renal IschemiaR01DK083291 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PADANILAM, BABU JOSEPH · 2010 to 2013
$1.3M
Mechanisms of selective glycolytic inhibition in ischemic kidney proximal tublesR56DK090332 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PADANILAM, BABU JOSEPH · 2012 to 2012
$150k
NIDDK NIH HHS R01 DK083291NIDDK NIH HHS R56 DK090332
6 · The paper itself

Abstract

In contrast to apoptosis and autophagy, necrotic cell death was considered to be a random, passive cell death without definable mediators. However, this dogma has been challenged by recent developments suggesting that necrotic cell death can also be a regulated process. Regulated necrosis includes multiple cell death modalities such as necroptosis, parthanatos, ferroptosis, pyroptosis, and mitochondrial permeability transition pore (MPTP)-mediated necrosis. Several distinctive executive molecules, particularly residing on the mitochondrial inner and outer membrane, amalgamating to form the MPTP have been defined. The c-subunit of the F1F0ATP synthase on the inner membrane and Bax/Bak on the outer membrane are considered to be the long sought components that form the MPTP. Opening of the MPTP results in loss of mitochondrial inner membrane potential, disruption of ATP production, increased ROS production, organelle swelling, mitochondrial dysfunction and consequent necrosis. Cyclophilin D, along with adenine nucleotide translocator and the phosphate carrier are considered to be important regulators involved in the opening of MPTP. Increased production of ROS can further trigger other necrotic pathways mediated through molecules such as PARP1, leading to irreversible cell damage. This review examines the roles of PARP1 and cyclophilin D in necrotic cell death. The hierarchical role of p53 in regulation and integration of key components of signaling pathway to elicit MPTP-mediated necrosis and ferroptosis is explored. In the context of recent insights, the indistinct role of necroptosis signaling in tubular necrosis after ischemic kidney injury is scrutinized. We conclude by discussing the participation of p53, PARP1 and cyclophilin D and their overlapping pathways to elicit MPTP-mediated necrosis and ferroptosis in acute kidney injury.

Indexed as

Acute Kidney InjuryAdenine Nucleotide Translocator 1AnimalsApoptosisCyclophilinsHumansMiceMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNecrosisPeptidyl-Prolyl Isomerase FPoly (ADP-Ribose) Polymerase-1Reactive Oxygen SpeciesSignal TransductionTumor Suppressor Protein p53Adenine Nucleotide Translocator 1CyclophilinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePARP1 protein, humanPeptidyl-Prolyl Isomerase FPoly (ADP-Ribose) Polymerase-1PPIF protein, mouseReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53BaxCyclophilin DNecroptosisp53PARP1Regulated necrosis

Identifiers

PMID27048819
PMCPMC5490387
OpenAlexW2333220158

What OpenQuestion holds

Textmetadata
LicenceTDM
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.