Abstract

All the living things, from single-cellular to multicellular organisms, are always exposed to certain environmental conditions. Sometimes, the environmental conditions are optimum for living, while the environment is very often harsh for the organisms, which is recognized as stress. During the processes of evolution, the organisms have developed various molecular mechanisms to protect themselves against the different environmental stresses. The collection of four papers in this issue presents timely developments in studies on the molecular mechanisms responding to environmental stresses such as cold temperature and DNA damage stress. It is well known that the brown adipose tissue has been used by animals to produce heat for resisting cold temperature, which is called thermogenesis. In thefirstarticle ofthis collection, Zhu’sgroupsystematically analyzed the molecular mechanism of thermogenesis in mice. They showed that a coldsensing molecule, transient receptor potential melastatin8(TRPM8), could result in the up-regulated expression ofuncoupling protein1(UCP1) in the brown adipose tissue under the treatment of menthol, a TRPM8 agonist. Upon mimicking, long-term cold exposure with chronic menthol administration, menthol significantly increased the core temperatures and locomotor activity in the wild-type mice, whereastheseeffectswereabsentinboththeknockout mice of TRPM8 and UCP1 genes, respectively. Theirworksfirst time reveal thatTRPM8channel triggers thermogenesis in a UCP1-dependent manner, which might be a new target for preventing obesity. Exposure to cold stress could induce cardiovascular dysfunction. In the second article, Ren’s group studied the role of the endothelin (ET) system in response to cold exposure environment with the wild-type and ETA receptor knockout mice. The authors showed that cold stress induced cardiac hypertrophy, depressed myocardial contractile capacity, changed behaviors of intracellular Ca 2+ ,

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