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. 2024 Jul 2;14(11):101034. doi: 10.1016/j.jpha.2024.101034

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© 2024 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 6 — Natural products target endoplasmic reticulum stress (ERS) mediated myocardial injury (MI) in heart failure, diabetic cardiomyopathy (DCM) and hypertensive. GRP78: glucose rregulated protein78; IRE1: inositol-requiring enzyme 1; PERK: protein kinase RNA (PKR)-like endoplasmic reticulum (ER) kinase; ATF6: activating transcription factor 6; ATF4: activating transcription factor 4; CHOP: CCAAT/enhancer-binding protein homologous protein; eNOS: endothelial-type nitricoxide synthase; NO: nitric oxide; CNPY2: cardiomyocyte-specific protein canopy homolog 2; NOX2: (nicotinamide adenine dinucleotide phosphate oxidase) NADPH oxidase 2; NOX4: NADPH oxidase 4; ROS: reactive oxygen species; COX2: cyclooxygenase-2; SIRT1: silencing information regulator 1; GRP78: glucose regulated protein78; JNK: c-Jun N-terminal kinase; AMPK: 5′ adenosine monophosphate-activated protein kinase; eIF2α: eukaryotic translation initiation factor 2α; MAPKs: mitogen-activated protein kinases; Bcl-2: BCL2 apoptosis regulator; AGEs: advanced glycosylation end products; TXNIP: thioredoxin interacting protein; NLRP3: NLR family fyrin domain containing 3; TNF-α: tumor necrosis factor-α; IL-1β: interleukin 1beta; IL-6: interleukin-6; ATF3: activating transcription factor 3.