Evidence map›Paper›PMID 25048553›Full record

ArticlePhotodiagnosis and photodynamic therapy2005

Mechanisms in photodynamic therapy: part two-cellular signaling, cell metabolism and modes of cell death.

Ana P Castano, Tatiana N Demidova, Michael R Hamblin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Photodiagnosis and photodynamic therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 222 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
222citing papers in PubMed, 2 pooled it
–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

222 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
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  8. Article
  9. Article
  10. Special Issue "Molecular Advances in Oncological Photodynamic Therapy".International journal of molecular sciences · 2026
    Article
  11. Review
  12. Review
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  14. Article
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  16. Combining NAD(P)H-FLIM and PLIM of Ir5 pH sensor to optimize photodynamic therapy through metabolic intracellular pattern segmentation.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  17. Review
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  20. Article

162 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

3 authors.

Ana P CastanoBAR314B, Wellman Center for Photomedicine, Massachusetts General Hospital, 50 Blossom Street, Bartlett 3, Boston, MA 02114, USA; Department of Dermatology, Harvard Medical School, USA.
Tatiana N DemidovaBAR314B, Wellman Center for Photomedicine, Massachusetts General Hospital, 50 Blossom Street, Bartlett 3, Boston, MA 02114, USA; Department of Cellular, Molecular and Developmental Biology, Tufts University, USA.
Michael R HamblinBAR314B, Wellman Center for Photomedicine, Massachusetts General Hospital, 50 Blossom Street, Bartlett 3, Boston, MA 02114, USA; Department of Dermatology, Harvard Medical School, USA.

Funding

Macrophage Targeted Photodynamic TherapyR01CA083882 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI HAMBLIN, MICHAEL R · 2002 to 2004
$740k
NCI NIH HHS R01 CA083882
6 · The paper itself

Abstract

Photodynamic therapy (PDT) has been known for over a hundred years, but is only now becoming widely used. Originally developed as a tumor therapy, some of its most successful applications are for non-malignant disease. In the second of a series of three reviews, we will discuss the mechanisms that operate in PDT on a cellular level. In Part I [Castano AP, Demidova TN, Hamblin MR. Mechanism in photodynamic therapy: part one-photosensitizers, photochemistry and cellular localization. Photodiagn Photodyn Ther 2004;1:279-93] it was shown that one of the most important factors governing the outcome of PDT, is how the photosensitizer (PS) interacts with cells in the target tissue or tumor, and the key aspect of this interaction is the subcellular localization of the PS. PS can localize in mitochondria, lysosomes, endoplasmic reticulum, Golgi apparatus and plasma membranes. An explosion of investigation and explorations in the field of cell biology have elucidated many of the pathways that mammalian cells undergo when PS are delivered in tissue culture and subsequently illuminated. There is an acute stress response leading to changes in calcium and lipid metabolism and production of cytokines and stress proteins. Enzymes particularly, protein kinases, are activated and transcription factors are expressed. Many of the cellular responses are centered on mitochondria. These effects frequently lead to induction of apoptosis either by the mitochondrial pathway involving caspases and release of cytochrome c, or by pathways involving ceramide or death receptors. However, under certain circumstances cells subjected to PDT die by necrosis. Although there have been many reports of DNA damage caused by PDT, this is not thought to be an important cell-death pathway. This mechanistic research is expected to lead to optimization of PDT as a tumor treatment, and to rational selection of combination therapies that include PDT as a component.

Identifiers

PMID25048553
PMCPMC4108176

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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.