Tuberculosis-diabetes comorbidities: Mechanistic insights for clinical considerations and treatment challenges

Figure 2 Mechanistic insights into the pathophysiologies of tuberculosis and diabetes mellitus interactions. Mtb: Mycobacterium tuberculosis; IFN: Interferon; HDT: Host-directed therapy; Eis: Enhanced intracellular survival; ESAT-6: Early secretory antigenic target; ESX-1: Secretion system-1; vitD3: Vitamin D3; ROS: Reactive oxygen species; LAP: Microtubule-associated protein light-chain 3-associated phagocytosis; VDR: Vitamin D receptor; CAMP: Cathelicidin antimicrobial peptide; iNOS: Inducible nitric oxide synthase; RAAS: Renin–angiotensin–aldosterone system; IR: Insulin resistance; PXR: Rifampicin activates pregnane X receptor; N-CoR: The nuclear receptor corepressor; PPAR: Peroxisome proliferator-activated receptor; RXR: Retinoic acid receptor; ORF: Open reading frame; OATP2: The sinusoidal transporters organic anion transporting protein 2; DDIs: Drug-drug interactions; RIF: Rifampin.