Skip to main content
. 2021 Dec 23;8:707336. doi: 10.3389/fcvm.2021.707336

Figure 1.

Figure 1

Novel inflammatory signaling pathways implicated in diabetic cardiomyopathy (DCM) pathogenesis and its possible pharmacological interventions. Inflammatory signaling has been proposed to be responsible for the development of DCM. It is activated by different pathways, including: (A) nuclear factor-kappa b (NF-κB) signaling activated by toll-like receptor 2 (TLR2), TLR4, and myeloid differentiation 2 (MD2)/TLR4 complex, (B) oxidative stress-induced autophagy, (C) oxidative stress, (D) activation of the NLR by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Moreover, some non-coding RNAs are described to (E) positively or (F) negatively regulate the inflammasome NLPR3. On the other hand, possible therapeutical strategies attenuating inflammatory signaling are illustrated as follows: (G) TLR2 depletion using siRNA TLR2 or TLR2-KO. (H) TLR4 depletion using siRNA TLR4 or TLR4-KO, TLR4 antagonist Rhodobacter sphaeroides LPS (Rs-LPS) and TLR4 blocker TAK242 and viral inhibitory peptide (VIPER), (I) decreasing NLRP3 by vaspin in an autophagy-dependent mechanism, (J) the inhibition of NLRP3 by metformin in an AMPK/mTOR-dependent manner, and (K) c-Jun N-terminal kinase (JNK) and spleen tyrosine kinase (SYK) inhibitor, melatonin, gypenosides (Gps), atorvastatin, SLGT2 inhibitor + P2Y12R antagonist, and SGLT2 inhibitor + DPP4 inhibitor.