Nonalcoholic steatohepatitis (NASH) is a leading cause of chronic liver disease, affecting 1.5%–6.5% of the world population. Currently, there are no FDA-approved drugs to treat this disease. Accumulating evidence suggests that metabolically hazardous visceral fat contributes to NASH progression by releasing fatty acids and proinflammatory mediators. Therefore, targeting adipose tissue to reduce adipose inflammation may provide an effective strategy to treat NASH. Another strategy is to target specific inflammatory mediators that are produced by adipose tissue and contribute to NASH progression. In this issue of the JCI, Liu, Xiang, et al. demonstrate that secreted protein acidic and rich in cysteine-like protein 1 (SPARCL1) was highly upregulated in adipose tissue and played a role in exacerbating NASH progression in a mouse model of NASH. Thus, inhibition of SPARCL1 may provide another attractive strategy to tackle NASH.

非酒精性脂肪性肝炎 (NASH) 是慢性肝病的主要原因，影响着世界人口的 1.5%–6.5%。目前，尚无 FDA 批准的药物来治疗这种疾病。越来越多的证据表明，对代谢有害的内脏脂肪通过释放脂肪酸和促炎介质而导致 NASH 进展。因此，针对脂肪组织来减少脂肪炎症可能为治疗 NASH 提供有效的策略。另一种策略是针对脂肪组织产生并导致 NASH 进展的特定炎症介质。在本期 JCI 中，Liu、Xiang 等人。证明富含半胱氨酸样蛋白 1 的酸性分泌蛋白 (SPARCL1) 在脂肪组织中高度上调，并在 NASH 小鼠模型中加剧 NASH 进展。因此，抑制 SPARCL1 可能为解决 NASH 提供另一种有吸引力的策略。