Signal Transducer and Activator of Transcription 3 (STAT3)

Where the papers sit

52 papers from the last 6 months study Signal Transducer and Activator of Transcription 3 (STAT3) directly · updated from PubMed 9 Oct 2026

• Inflammatory STAT3 Signaling

  STAT3 and NF-κB inhibition is being pursued to control inflammatory injury in liver, bone, heart, nervous tissue and transplantation. BP-1-102 and Bruceine D suppress NFATc1-linked osteoclastogenesis, while succinic acid and a dihydroxyacetophenone analog expose distinct ways to impair hepatic repair or acute liver injury. SH-17 targets both Tyr705 and Ser727 phosphorylation, broadening intervention beyond a single STAT3 site. Transplant rejection profiling and reporter-mouse atlases emphasize timing and cell context as unresolved determinants.

  10 papers · 19.2%

• Cancer Immunogenic Cell Death

  STAT3 inhibition is increasingly being connected to immunogenic or regulated tumor cell death rather than growth arrest alone. Ferroptosis, cuproptosis and apoptosis recur alongside CD8-positive T-cell activity, PD-1 resistance and metabolic vulnerabilities such as the PD-L1–PDK4/GLS axis. Hydrazone, allosecurinine and stattic-based agents provide preclinical routes to STAT3 blockade, while atranorin links LUCAT1 suppression to ferroptosis. The open question is whether these death programs can reliably convert resistant tumors into durable immunotherapy responders.

  10 papers · 19.2%

• STAT3-Driven Cancer Progression

  STAT3-directed agents are moving from pathway inhibition toward direct degradation and multitarget blockade in solid tumors. SD-2301 is reported to produce complete tumor regression after single administration, while STAT3/HDAC, STAT3/NF-κB and NQO1/STAT3/HDAC compounds address transcriptional and epigenetic cooperation. miR-124 vesicles, SCP-7 targeting Cys328 and evodiamine suppress growth, apoptosis or cachexia-associated muscle loss in preclinical models. Resistance and biomarker selection remain open, including SAT1-associated enzalutamide sensitivity in prostate cancer.

  9 papers · 17.3%

• Metabolic Inflammation and Organ Injury

  JAK2/STAT3, NF-κB and oxidative-stress networks are being targeted across diabetic cardiomyopathy, kidney injury, wound healing and vascular inflammation. Hydrogen sulfide, dapagliflozin and artesunate are linked to tissue protection through pathway suppression or remodeling, while extracellular-vesicle miRNAs can worsen diabetic renal injury. Clovamide analogues and a lysosome-gated TA-Fe nanoplatform extend this strategy to colitis and diabetic wounds. The field is moving toward network-level control of inflammation and autophagy, but organ-specific mechanisms remain unresolved.

  7 papers · 13.5%

• Inflammation and Fibrosis

  IL-6/JAK/STAT3 signaling is being linked to fibrotic remodeling across kidney, lung, thyroid eye disease and scleroderma. Diosgenin nanoconjugates, Yupingfeng San, digoxin and combined retinoic acid–rosiglitazone approaches aim to reduce fibrosis by restoring mitochondrial function or suppressing HIF-1α and Th17 activity. Sinomenine extends pathway modulation to astrocyte reactivity and neuropathic pain, while CDK8/19 inhibitors target IL-6-dependent lymphoma. Shared pathway biology is clear, but disease-specific mechanisms and clinical translation remain open.

  6 papers · 11.5%

• Others — Metabolic and Immune Signaling

  AKT and JAK-STAT signaling recur across metabolic disease, cancer drug resistance, neuroinjury, infection and autoimmunity, but no single clinical direction unifies the group. Evodiamine and FGF21-based approaches target insulin or leptin resistance, while exosomal p-AKT is linked to doxorubicin resistance in breast cancer. Other work tests propranolol after TBI, CSF1R blockade with CDK4/6 inhibition, and pathway changes in celiac disease. The common thread is mechanistic pathway mapping rather than a shared therapeutic strategy.

  10 papers · 19.2%