Tissue fibrosis is initially an adaptive response to organ injury, but eventually, parenchymal scarring and subsequent cellular dysfunction and organ failure ensue. Few therapies currently exist for fibrosis, especially those that target fibrogenesis. Galectin-3 (Gal-3) is a member of the lectin family of proteins, is produced predominantly by macrophages, and has essential functions in inflammation and angiogenesis. Gal-3 is activated in fibrotic models and abnormally elevated in fibrotic patients. Gal-3 inhibitors help to ameliorate or prevent fibrosis. For this review, we searched for original articles and reviews published between Jul 1, 2014, and Nov 1, 2019, using the following search terms (or combination of words) in PubMed: “galectin 3”, “fibrosis”, “heart”, “cardiac”, “liver”, “hepatic”, “lung”, “pulmonary”, “kidney”, and “renal”.

Circulatory shock is characterized by a decrease in oxygen delivery to the tissues associated with impairment in oxygen metabolism and tissue hypoxia. Clinical and biological signs of impaired tissue perfusion and tissue hypoxia are used as bedside to detect circulatory failure and trigger resuscitation procedures. The most popular signs of tissue hypoperfusion include mean arterial pressure, capillary refill time and mottling score, central venous oxygen saturation (ScvO₂), veno-arterial difference in PCO₂ (PvaCO₂), microcirculation assessment, and lactate. Both the severity and duration of the alterations in any of these variables are associated with a poor outcome so that it sounds logical to trigger therapy based on these. Using these variables as target for therapy is much more complex. Some of the limits for using some of these variables as targets include an incertitude about the target to reach (should we aim at normalizing or improving the variable, and by how much?) and the time lag between resolution of impaired tissue perfusion/hypoxia and normalization of the variable. The ideal target variable should have a well-defined end point and a rapid response time. Interestingly, hemodynamic resuscitation targeting these variables gave variable results. In this review, we will discuss the interest and limitations of the above-mentioned indices of tissue perfusion and hypoxia as trigger as well as end point of resuscitation in critically ill patients.