Table 1.

Comparative analysis of Fanlian Huazhuo formula and existing metabolic associated steatotic liver disease treatments: Mechanisms, efficacy, and future research directions¹

Aspect	Fanlian Huazhuo formula	Existing metabolic associated steatotic liver disease treatments
Mechanism of action	Modulates autophagy and lipid synthesis signaling pathways[1]	Varies: Inflammation modulation, autophagy regulation, lipid metabolism, and gut microbiota management[1-10]
Key pathways targeted	Autophagy, lipid synthesis pathways[1]	NF-κB/NLRP3[2], IRE1-α/IKKβ/NF-κB[6], AMPK[7], TLR4/NF-κB[7], PPARα-RXRα[11]
Efficacy	Alleviates high-fat diet-induced metabolic associated steatotic liver disease; reduces hepatic steatosis and inflammation[1]	Demonstrated effectiveness in reducing liver fat, inflammation, and improving liver function[3,6,9]
Comparison with other treatments	Promising in balancing autophagy and lipid metabolism, potentially offering a unique approach compared to conventional drugs	Existing treatments such as Huanglian-Hongqu[2], Fufang Fanshiliu Decoction[3], and Gynostemma pentaphyllum[4] show efficacy in different pathways, suggesting a multi-faceted approach
Clinical evidence	Evidence from animal studies; human clinical trials are needed[1]	Extensive clinical and preclinical evidence supports their efficacy[2,3]
Current limitations	Lack of extensive human clinical trial data; mechanism needs further elucidation[1]	Some treatments may have limited long-term efficacy or side effects; continued research needed for optimization[2,5]
Future research directions	Further human clinical trials to validate efficacy; exploration of long-term effects and safety profiles[1]	Ongoing studies to explore new drug combinations, personalized treatments, and mechanism-based therapies. Research into combination therapies and natural products is also ongoing[6,12]

¹This table presents a comparative analysis of Fanlian Huazhuo formula (FLHZF) and other treatments for metabolic associated steatotic liver disease (MASLD).

It outlines the mechanisms through which FLHZF and other therapies exert their effects on MASLD, focusing on key signaling pathways and molecular targets. FLHZF is noted for its impact on autophagy and lipid synthesis pathways, while other treatments address various pathways, including nuclear factor-kappa B (NF-κB)/NOD-like receptor protein 3, inositol-requiring enzyme 1 alpha/inhibitor of kappa B kinase beta/NF-κB, AMP-activated protein kinase, Toll-like receptor 4/NF-κB, and peroxisome proliferator-activated receptor alpha/retinoid X receptor alpha. The table also summarizes the observed efficacy of these treatments in improving hepatic steatosis, inflammation, and overall liver function. It highlights how FLHZF compares with other therapies in terms of approach and potential benefits, the level of clinical evidence supporting each treatment, and current limitations. Future research directions are suggested to enhance understanding and effectiveness, emphasizing the need for further clinical trials and exploration of combination therapies.