Molecular mechanisms of photodynamic therapy

被引：78

作者：

Ortel, Bernhard ^{[1
]}

Shea, Christopher R. ^{[1
]}

Calzavara-Pinton, Piergiacomo ^{[2
]}

机构：

[1] Univ Chicago, Med Ctr, Dermatol Sect, Chicago, IL 60637 USA

[2] Univ Brescia, Dept Dermatol, I-25123 Brescia, Italy

来源：

FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷

关键词：

Photodynamic; Photosensitization; Cancer; Apoptosis; Immunity; Inflammation; Porphyrin; Aminolevulinic; Tetrapyrrole; Review; NF-KAPPA-B; MEDIATED OXIDATIVE STRESS; APOPTOSIS-INDUCING FACTOR; ENDOTHELIAL GROWTH-FACTOR; AUTOPHAGIC CELL-DEATH; 5-AMINOLEVULINIC ACID; CYTOCHROME-C; MATRIX METALLOPROTEINASES; IMMUNE-RESPONSE; CROSS-LINKING;

D O I：

10.2741/3520

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Despite its more than 100-year history in experimental and clinical use, photodynamic therapy (PDT) is only starting to be appreciated for its full potential. PDT combines a photosensitizer (PS) and light in the presence of oxygen to treat cancer and other disorders. This manuscript reviews molecular mechanisms that have been evaluated over the past years for the effects of PDT at the cellular level as well as in therapeutic settings in vivo. The availability of multiple PS with different structures and functional properties makes PDT an extremely versatile and, conversely, a challenging approach to cancer therapy. The advancing understanding of molecular pathways helps to design improved regimens. As most cancers are being treated with combination therapies, PDT is being integrated into rationally designed combined regimens that exploit molecular responses to PDT for improved efficacy.

引用

页码：4157 / 4172

页数：16

共 164 条

[1]

AGARWAL ML, 1993, CANCER RES, V53, P5897

[2]

AGARWAL ML, 1991, CANCER RES, V51, P5993

[3]

Bellnier DA, 2003, CANCER RES, V63, P7584

[4] Photofrin photodynamic therapy for treatment of AIDS-related cutaneous Kaposi's sarcoma [J].

Bernstein, ZP ;

Wilson, BD ;

Oseroff, AR ;

Jones, CM ;

Dozier, SE ;

Brooks, JSJ ;

Cheney, R ;

Foulke, L ;

Mang, TS ;

Bellnier, DA ;

Dougherty, TJ .

AIDS, 1999, 13 (13) :1697-1704

[5] Structure and biodistribution relationships of photodynamic sensitizers [J].

Boyle, RW ;

Dolphin, D .

PHOTOCHEMISTRY AND PHOTOBIOLOGY, 1996, 64 (03) :469-485

[6] Multiple components of photodynamic therapy can phosphorylate akt [J].

Bozkulak, Ozguncern ;

Wong, Sam ;

Luna, Marian ;

Ferrario, Angela ;

Rucker, Natalie ;

Gulsoy, Murat ;

Gomer, Charles J. .

PHOTOCHEMISTRY AND PHOTOBIOLOGY, 2007, 83 (05) :1029-1033

[7] DARK INDUCTION OF HEME OXYGENASE MESSENGER-RNA BY HEMATOPORPHYRIN DERIVATIVE AND ZINC PHTHALOCYANINE - AGENTS FOR PHOTODYNAMIC THERAPY [J].

BRESSOUD, D ;

JOMINI, V ;

TYRRELL, RM .

JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY, 1992, 14 (04) :311-318

[8] Deficiency in apoptotic effectors bax and bak reveals an autophagic cell death pathway initiated by photodamage to the endoplasmic reticulum [J].

Buytaert, E. ;

Callewaert, G. ;

Vandenheede, J. R. ;

Agostinis, P. .

AUTOPHAGY, 2006, 2 (03) :238-240

[9] Molecular effectors of multiple cell death pathways initiated by photodynamic therapy [J].

Buytaert, Esther ;

Dewaele, Michael ;

Agostinis, Patrizia .

BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 2007, 1776 (01) :86-107

[10] Role of endoplasmic reticulum depletion and multidomain proapoptotic BAX and BAK proteins in shaping cell death after hypericin-mediated photodynamic therapy [J].

Buytaert, Esther ;

Callewaert, Geert ;

Hendrickx, Nico ;

Scorrano, Luca ;

Hartmann, Dieter ;

Missiaen, Ludwig ;

Vandenheede, Jackie R. ;

Heirman, Ingeborg ;

Grooten, Johan ;

Agostinis, Patrizia .

FASEB JOURNAL, 2006, 20 (02) :756-+

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