CHEST Guidelines-Linking-Genetics-to-ARDS-Pathogenesis

Linking-Genetics-to-ARDS-Pathogenesis_chest

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The document discusses the linkage between genetic factors and Acute Respiratory Distress Syndrome (ARDS), specifically focusing on the role of platelets in its pathogenesis. ARDS, identified by damaged alveolar-capillary barriers and heightened inflammatory responses, has increasingly been linked to activated clotting pathways and platelet activity. In critical illnesses such as sepsis, mechanisms activating platelets lead to inflammation and increased permeability, thereby aggravating ARDS.<br /><br />Recent studies have shown the potential of therapeutically targeting platelet activation. In mouse models, the inhibition of platelet-neutrophil interactions has shown protective effects against lung injury, and human studies link anti-platelet medications like aspirin and clopidogrel to a reduced ARDS risk and mortality. Ongoing research, including the Lung Injury Prevention Study with Aspirin (LIPS-A), aims to evaluate such therapeutics in preventing ARDS.<br /><br />The article also highlights a study by Wei and colleagues identifying a novel genetic variant in LRRC16A associated with ARDS risk, pointing out that platelet count may serve as a mediator in this risk. However, it cautions that the study only assessed platelet count at ICU admission, leaving unanswered questions regarding platelet production and function. Further research is suggested to understand better how variations in LRRC16A affect platelet and ARDS biology, potentially offering new therapeutic targets.<br /><br />This work underscores the importance of platelets in ARDS and suggests broader research efforts should focus on the genetic underpinnings and mechanisms influencing platelet function in critical illnesses. The study represents a promising direction for enhancing the prevention and treatment of ARDS by leveraging genetic insights.

Keywords

ARDS

genetic factors

platelets

pathogenesis

inflammation

platelet activation

aspirin

LRRC16A

therapeutic targets

lung injury