Background: Although hypothermia protects against the renal injury induced by ischemia reperfusion, the detailed molecular pathway(s) involved in the process remain unknown. Proliferator-activated receptor-gamma coactivator 1alpha (PGC-1α) is known to protect against renal injury. Furthermore, hypothermia may induce PGC-1α in the brain and the kidneys. We evaluated the role of PGC-1α in hypothermia protection against renal ischemia reperfusion injury (IRI). Methods: We prepared a fibrosis model by inducing ischemia reperfusion injury. C57BL/6 mice were divided into the following groups: sham mice and ischemia reperfusion injury mice (37°C vs. 32°C). The kidneys were harvested 20 minutes after the induc- tion of renal ischemia and on day 1, day 3, day 7, and after IRI. Fibrosis markers and the renal injury score were evaluated. Results: The blood urea nitrogen levels, and serum creatinine levels, and the histologic renal injury scores were significantly lower in the 32°C IRI groups than in the 37°C ischemia reperfusion injury groups. The protein levels of fibrosis markers were sig- nificantly decreased, while the bone morphogenetic protein 7 (BMP7) and PGC-1α level was significantly increased in the 32°C ischemia reperfusion injury mice group. Hypothermia increased the PGC-1α both, in vivo and in vitro. Knock down of PGC-1α ex-pression increased in vitro renal fibrosis. Conclusions: Hypothermia ameliorates renal function deterioration and renal fibrosis in renal IRI mice kidneys. Moreover, hypo-thermia increases PGC-1α in renal IRI mice kidneys. Therefore, PGC-1α may play a role in hypothermic protection in renal fibrosis following IRI.