PPARA (Peroxisome Proliferator Activated Receptor Alpha)

Furthermore, PS reduced hepatic pro-inflammatory cytokine mRNA levels: tumor necrosis factor α(tnf-α), cyclooxygenase 2 (cox-2), and interleukins (il-6, il-1β). In conclusion, dietary inclusion of 0.006%-0.018% PS effectively enhanced growth and antioxidant capacity, altered lipid handling, and affected transcriptional inflammatory responses.

PF effectively attenuated hepatic metabolic dysregulation, inflammation, and fibrotic activation through inhibition of this pathway. Our work provided the first evidence establishing the SYK/SH3BP2 signaling axis as a pivotal pathway in MASLD progression, unveiling novel therapeutic targets while furnishing a mechanistic foundation for PF's potential application in MASLD treatment.

Mechanistic studies demonstrated that ZFP2 modulates lipid metabolism through the PPARα/LXRα/ABCG8 signaling pathway, enhancing lipid catabolism and reducing lipid accumulation. These findings underscore the potential of ZFP2 as a natural hypolipidemic agent and support the development of fingered citron polysaccharide as functional food ingredients for managing lipid-related disorders.

Considering the availability of PPAR modulatory drugs, it may be an important therapeutic target. In addition, the meticulous examination of the brain invasion still holds significant promise for prognostication.

Fenofibrate improves endothelial-dependent relaxation and NO production in HFD-induced obese mice, likely through activation of the LKB1/AMPK/Akt pathway. The suppression of hepatic GRK2 activity by fenofibrate may contribute to better lipid metabolism, thereby promoting the recovery of vascular function.

This effect is accompanied by coordinated modulation of PPARα/NF-κB, sirtuin, autophagy, and MMP pathways. These findings support further evaluation of carvacrol as a microenvironment-directed adjunct in breast cancer therapy.

Over time, persistent CS under steatotic conditions leads to mitochondrial dysfunction and suppression of fatty acid oxidation (FAO), while the senescence-associated secretory phenotype (SASP), largely driven by nuclear factor-kappa B (NF-κB) signaling, promotes chronic hepatic inflammation. By framing LDs as active modulators of senescence-associated signaling rather than passive lipid stores, this review highlights how disruption of senescence-lipid feedback loops may represent a disease-modifying opportunity in MASLD progression.

This allows treatment to be carried out in an outpatient setting, including for elderly and comorbid patients. Triple transcriptional modulation, facilitated by epigenetic modelling with azacitidine, targets reprogramming of non-oncogene addiction networks in AML, re-establishing functionally active, closely interrelated myeloid hallmarks and AML cell death genome-agnostically.

these findings indicate that Complex I modulation may represent a promising strategy to counteract MASLD progression toward MASH.

This narrative review highlights the novelty of consolidating scattered preclinical data on AA, a lesser-known natural compound in pharmacology, to increase awareness of its multifaceted therapeutic potential. Its utility lies in guiding future research toward optimized derivatives and formulations, potentially bridging traditional medicine with modern therapeutics for conditions like cancer, inflammation, and infections, while identifying key gaps for interdisciplinary efforts.

Sesamin exhibits promising antiproliferative and pro-apoptotic activities against DU145 prostate cancer cells. Its potential to act as a G1-phase-specific chemotherapeutic agent via a p53-independent mechanism warrants further investigation and development as a natural candidate for prostate cancer therapy.