Helicobacter pylori and diabetic complications: Stronger evidence for the interlink

Figure 1 Putative mechanisms involved in developing cardiovascular disease and metabolic dysfunction-associated fatty liver disease in patients with Helicobacter pylori infection. H. pylori: Helicobacter pylori; IL: Interleukin; TNF-α: Tumor necrosis factor alpha; ICAM: Intercellular adhesion molecule; VCAM-1: Vascular cell adhesion molecule-1; NF-κB: Nuclear factor kappa B; JNK: C-Jun N-terminal kinase; TGF-β: Transforming growth factor beta; AMPK: Adenosine monophosphate phosphate-activated protein kinase; SREBP1: Sterol regulatory element-binding protein 1; PPARα: Peroxisome proliferator-activated receptor alpha; MASH: Metabolic dysfunction-associated steatohepatitis; LPS: Lipopolysacharide; IgA: Immunoglobulin A; IgG2: Immunoglobulin G2; TXA2: Thromboxane A2; PGE2: Prostaglandin E2; TC: Total cholesterol; LDL: Low density lipoprotein; TG: Triglyceride; HDL: High density lipoprotein; hs-CRP: Highly sensitive C-reactive protein; HOMA-IR: Homeostatic model assessment for estimating insulin resistance; ROS: Reactive oxygen species; LPL: Lipoprotein lipase; ER: Endoplasmic reticulum; MAFLD: Metabolic-dysfunction associate fatty liver disease.