KLF4
KLF4 (Krüppel-like factor 4) is a transcription factor implicated in the regulation of epithelial integrity, endothelial function, immune-cell state, vascular smooth-muscle phenotype, and cellular responses to oxidative stress and ferroptosis.
KLF4 (Krüppel-like factor 4) is a transcription factor implicated in the regulation of epithelial integrity, endothelial function, immune-cell state, vascular smooth-muscle phenotype, and cellular responses to oxidative stress and ferroptosis. In the studies summarized here, KLF4 functions as a context-dependent regulator: its activity is associated with transcription of tight-junction genes, mitochondrial respiratory-chain programs, and signaling pathways involving β-catenin, SIRT3, and glutathione peroxidase 4 (GPX4).
KLF4 has been investigated as a target in cancer progression and immunity, aging-related neurovascular dysfunction, cardiovascular disease, diabetic nephropathy, and cellular therapies. The reported work uses approaches including RNA sequencing, CRISPR-Cas methods, chromatin immunoprecipitation, luciferase and RNA immunoprecipitation assays, western blotting, and functional cell assays. Collectively, these studies place KLF4 at the intersection of epithelial barrier regulation, the blood–brain barrier, oxidative stress, ferroptosis, tumor microenvironment signaling, and CAR-T-cell function.
Rebuilt from PubMed 10 Sept 2026 · no new papers today
Where the papers sit
9 papers study klf4 directly. Those 9 do not group into themes. KLF4 recurs as a regulatory factor in ferroptosis, immune evasion, vascular dysfunction, cancer metastasis, and CAR-T exhaustion. The studies share KLF4-related biology but no common disease or mechanistic direction. They are no more alike than papers drawn from anywhere in the corpus.
Recent Findings on KLF4
Gastric cancer metastasis and tight-junction restoration: A study investigated how angiotensin II type 1 receptor (AT1R) blockade affects gastric cancer metastasis. Global RNA sequencing, CRISPR/Cas9 gene deletion, chromatin immunoprecipitation, and functional assays indicated that angiotensin II produced predominantly by cancer cells in the tumor microenvironment suppresses KLF4 through cancer-cell AT1R. Reduced KLF4 was associated with decreased transcription of the tight-junction genes CLDN1, CLDN3, CLDN4, and TJP1, thereby reducing tight-junction protein synthesis. The findings connect KLF4 to epithelial integrity and suggest that AT1R blockade can counter this pathway and restore tight-junction-associated molecular programs 42081962May.
Hypoxia, endothelial exosomes, and vascular smooth-muscle switching: In a study of hypoxia-induced endothelial exosomal effects, bioinformatic analysis, luciferase assays, and RNA immunoprecipitation assays were used to examine the MSTRG.12883.2/miR-632/KLF4 axis. The work investigated how an endothelial exosome-associated noncoding RNA pathway participates in ox-LDL-induced phenotypic switching of vascular smooth muscle cells, a process relevant to atherosclerosis and cardiovascular disease 42107690May.
Diabetic nephropathy and ferroptosis: Researchers examined whether miR-145-5p regulates high-glucose-induced ferroptosis and injury in renal tubular epithelial cells through the KLF4/SIRT3/GPX4 signaling axis. The study therefore positioned KLF4 within a pathway linking microRNA regulation to mitochondrial or metabolic protection, glutathione-dependent antioxidant defense, and GPX4-associated control of ferroptosis in diabetic nephropathy 42494277Jul.
Esophageal cancer, immune evasion, and immunotherapy: A study reported that downregulation of KLF4 during esophageal cancer development is essential to an immune-decisive process associated with cancer progression. Its findings linked reduced KLF4 expression with immune evasion and impaired immunotherapy, including anti-PD-1 therapy, identifying KLF4 loss as a feature relevant to tumor–immune interactions 42493491Jul.
Endothelial KLF4 and aging-related neurovascular dysfunction: Endothelial cells throughout the body were described as being enriched for KLF4. The study investigated the consequences of endothelial KLF4 depletion for age-related neurovascular dysfunction and neuropsychiatric impairment, placing KLF4 in the regulation of endothelial function and blood–brain barrier-associated pathology 42313933Jun.
Epigenetic drug combinations in colon cancer: A study of valproic acid combined with zebularine examined regulation of KLF4 and β-catenin expression in colon cancer cells. Gene-expression analysis reported an approximately twofold increase in KLF4 expression in SW480 cells and an approximately 22-fold increase in DLD-1 cells following the experimental treatment strategy. The work supports investigation of combined epigenetic drug treatment as a means of modifying KLF4-associated and nuclear β-catenin-related cancer-cell programs 42224286Jun.
KLF4 overexpression in CAR-T cells: KLF4 overexpression was investigated as a strategy to improve the antitumor potency of chimeric antigen receptor T (CAR-T) cells. The reported conclusion was that increased KLF4 expression enhanced CAR-T antitumor activity by preventing T-cell exhaustion, identifying KLF4 as a potential regulator of therapeutic immune-cell state 42161404May.
Mitochondrial function, neuronal ferroptosis, and cognitive decline: A study of the ATP11B–YAP axis reported that ATP11B regulates chromatin accessibility of KLF4 at genes encoding mitochondrial respiratory-chain complexes. This mechanism was examined in relation to mitochondrial respiratory function, neuronal ferroptosis, and age-related cognitive decline, linking KLF4-dependent chromatin regulation to neuronal oxidative and metabolic stress 42002550Apr.
Written from 9 PubMed abstracts, each one cited by PMID above. Published: 2026-09-10. Drafted by language models from published abstracts; not medical advice.