Hepatic ischemia-reperfusion injury and therapeutic strategies to alleviate cellular damage

Dogan S., Aslan M.

HEPATOLOGY RESEARCH, cilt.41, sa.2, ss.103-117, 2011 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 41 Sayı: 2
  • Basım Tarihi: 2011
  • Doi Numarası: 10.1111/j.1872-034x.2010.00765.x
  • Dergi Adı: HEPATOLOGY RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.103-117
  • Anahtar Kelimeler: hepatocyte, injury, ischemia, reperfusion, NITRIC-OXIDE SYNTHASE, FACTOR-KAPPA-B, N-TERMINAL KINASE, MITOCHONDRIAL PERMEABILITY TRANSITION, WARM ISCHEMIA/REPERFUSION INJURY, PLATELET-ACTIVATING-FACTOR, RAT-LIVER TRANSPLANTATION, NECROSIS-FACTOR-ALPHA, HEAT-SHOCK PROTEINS, TOLL-LIKE RECEPTORS
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Hepatic ischemia-reperfusion injury and therapeutic strategies to alleviate cellular damage.

Dogan S1, Aslan M.

Abstract

Warm hepatic ischemia-reperfusion injury is a significant medical problem in many clinical conditions such as liver transplantation, hepatic surgery for tumor excision, trauma and hepatic failure after hemorrhagic shock. Partial or, mostly, total interruption of hepatic blood flow is often necessary when liver surgery is performed. This interruption of blood flow is termed "warm ischemia" and upon revascularization, when molecular oxygen is reintroduced, the organ undergoes a process called "reperfusion injury" that causes deterioration of organ function. Ischemia reperfusion results in cellular damage and tissue injury associated with a complex series of events. Pathophysiological mechanisms leading to tissue injury following ischemia-reperfusion will be discussed and therapies targeted to reduce liver damage will be summarized within this review.