Leptina e disturbi polmonari acuti

Leptin, an adipokine primarily produced in white adipose tissue, plays a crucial role in metabolism, immunity, and inflammation. Originally identified as a satiety hormone, leptin is also synthesized in various tissues, including the lungs, where it regulates immune responses by binding to the ObR receptor and activating pathways like JAK–STAT3 and PI3K. Functioning as a cytokine‐like hormone, leptin modulates innate and adaptive immunity by promoting T and B cell proliferation, macrophage activation, and chemokine secretion. In lung physiology, leptin contributes to maturation and alveolar development, but its role in acute lung disorders such as acute respiratory distress syndrome (ARDS) remains controversial. The “obesity paradox” suggests that obese patients may be protected against ARDS, potentially due to hyperleptinemia‐driven immune modulation, enhanced neutrophil recruitment, and improved alveolar macrophage function. However, obesity‐induced leptin resistance may impair these protective effects. Conflicting animal studies on leptin's role in acute lung injury (ALI) further complicate its understanding, with some showing protection and others increased susceptibility to lung damage. Further research is needed to clarify leptin's influence on lung inflammation and its interplay with metabolic disorders like obesity, which could inform targeted therapeutic strategies for ARDS and other pulmonary diseases. Leptin, an adipocyte‐derived cytokine‐like hormone, plays a crucial role in metabolism and immunity but its role in acute lung disorders such as acute respiratory distress syndrome (ARDS) remains controversial. Elucidating leptin's role in lung inflammation, and its interplay with metabolic disorders like obesity, will help designing therapeutical strategies in ARDS.