Liver fibrosis is a common pathological process of chronic liver diseases, including viral hepatitis and alcoholic liver disease, and ultimately progresses to irreversible cirrhosis and cancer. Hepatic stellate cells (HSCs) are activated to produce amounts of collagens in response to liver injury, thus triggering the initiation and progression of fibrogenesis. Natural killer (NK) cells serve as the essential component of hepatic innate immunity and are considered to alleviate fibrosis by killing activated HSCs. Current antifibrotic interventions have improved fibrosis, but fail to halt its progression in the advanced stage. Clarifying the interaction between NK cells and HSCs will provide clues to the pathogenesis and potential therapies for advanced liver fibrosis.

Liver fibrosis is the common pathological change of chronic liver diseases characterized by increased deposition of extracellular matrix and reduced matrix degradation. In response to liver injury caused by a variety of pathogenic agents, such as virus and alcohol, hepatic stellate cells (HSCs) are differentiated into myofibroblast-like cells and produce excessive collagens, thus resulting in fibrogenesis. Natural killer (NK) cells are the essential innate immune cells in the liver and generally control fibrosis by killing activated HSCs. This review briefly describes the fibrogenesis process and the phenotypic features of hepatic NK cells. Besides, it focuses on the antifibrotic mechanisms of NK cells and explores the potential of activating NK cells as a therapeutic strategy for the disease.

Melanoma is the most aggressive form of skin cancer with the poorest prognosis and its pathogenesis has yet to be fully elucidated. As key factors that regulate cellular homeostasis, both reactive oxygen species (ROS) and autophagy are involved in the development of melanoma, from melanomagenesis to progression and drug resistance. However, the interaction between ROS and autophagy in the etiology and treatment of melanoma is not well characterized. The present review examined the production of ROS and the role of oxidative stress in melanoma, and summarized the role of ROS‑mediated autophagy in melanomagenesis and melanoma cell fate decision following treatment with various anticancer drugs. The present findings may lead to a better understanding of the pathogenesis and progression of melanoma, and suggest promising treatment options for this disease.

Carbon monoxide (CO), a by-product released during the degradation of heme by heme oxygenases (HOS EC 1.14.99.3) in animals, plays a major role as neurotransmitter, regulator of sinusoidal tone, inhibitor of platelet aggregation, and suppressor of acute hypertensive response, and most of above effects are similar to or mediated by nitric oxide (NO), another signal molecule in both the animal and plant kingdoms. Previous result demonstrated that NO could act as a promoter of plant cell elongation, acting similarly to IAA, inducing morphogenetic responses leading to expansion in plant tissues. Recent observations revealed that CO is an inducer of cell expansion in wheat root segments, acting similarly to IAA and NO. Evidence also indicated that IAA could result in either the potent induction of HO-1 transcript or endogenous CO releasing in wheat root segments. Additionally, our results suggested that above CO signaling might be related to NO/cGMP, Ca2+ and even ROS-dependent pathways. In this addendum, combined with other previous results, we further proposed a possible hypothesis for CO signaling role in regulation of plant root development induced by auxin.

With the growing interest to harness cancer metabolism and energy reprogramming, this mini review aimed to explain the metabolic programming revealing the mechanisms regarding the treatment resistance. This mini review summarized the prominent cancer metabolic reprogramming on macromolecules. In addition, metabolic reprogramming explaining immune response and treatment resistance as well as energy reprogramming mechanisms are briefly discussed. Finally, some prospects in MR for reversing cancer drug resistance are highlighted.