Acute lung injury (ALI) is a severe condition characterized by an inflammatory response and increased vascular permeability, with its pathological mechanisms closely associated with the dysfunction of vascular smooth muscle cells (VSMCs). The present study investigates the molecular mechanisms through which lactate dehydrogenase A (LDHA) influences the inflammatory response in ALI by modulating VSMC metabolic reprogramming. It was observed that under pathological conditions, hypoxia and the inflammatory microenvironment significantly upregulate LDHA expression in lung VSMCs via the activation of the hypoxia-inducible factor (HIF) signaling pathway. The LDHA-mediated Warburg effect not only provides energetic support to VSMCs but also exacerbates inflammatory responses through both direct and indirect mechanisms. This review highlights the critical role of LDHA as a metabolic-inflammatory nexus in ALI and offers a theoretical foundation for targeting LDHA to regulate metabolic reprogramming as a means to mitigate the progression of ALI. Future research will further investigate the specific mechanisms by which LDHA regulates VSMC metabolic reprogramming and will seek to identify effective intervention strategies.
Lian et al. (2026) studied this question.