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Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.

Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.

期刊: Genes 日期: 2026-06-03 PMID: 42353816 DOI: 10.3390/genes17060657 浏览: 10
作者: Santoyo-Suárez MG, García-Loredo JA, Mares-Montemayor JD, Delgado-Gallegos JL, Garza-Ocañas L, Rodríguez-Nuñez O, Soto-Dominguez A, Camacho-Morales A, Zapata-Morin P, Padilla-Rivas GR
MG, S.S., JA, G.L., JD, M.M., JL, D.G., L, G.O., O, R.N., A, S.D., A, C.M., P, Z.M., & GR, P.R. (2026). Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.. Genes. https://doi.org/10.3390/genes17060657
MG SS, JA GL, JD MM, JL DG, L GO, O RN, et al. Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.. Genes. 2026; doi: 10.3390/genes17060657
MG SS, JA GL, JD MM, et al. Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.[J]. Genes. 2026. DOI: 10.3390/genes17060657.
@article{mg2026,
  author = {Santoyo-Suárez MG and García-Loredo JA and Mares-Montemayor JD and Delgado-Gallegos JL and Garza-Ocañas L and Rodríguez-Nuñez O and Soto-Dominguez A and Camacho-Morales A and Zapata-Morin P and Padilla-Rivas GR},
  title = {Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.},
  journal = {Genes},
  year = {2026},
  doi = {10.3390/genes17060657},
  note = {PMID: 42353816},
}
TY  - JOUR
AU  - Santoyo-Suárez MG
AU  - García-Loredo JA
AU  - Mares-Montemayor JD
AU  - Delgado-Gallegos JL
AU  - Garza-Ocañas L
AU  - Rodríguez-Nuñez O
AU  - Soto-Dominguez A
AU  - Camacho-Morales A
AU  - Zapata-Morin P
AU  - Padilla-Rivas GR
TI  - Temporal Orchestration of Krüppel-like Factors During Cardiac Remodeling Following Isoproterenol-Induced Myocardial Injury.
T2  - Genes
PY  - 2026
DO  - 10.3390/genes17060657
AN  - PMID:42353816
ER  - 

摘要

Background: Myocardial infarction triggers a complex remodeling process involving inflammation, hypertrophy, fibrosis, and electrical adaptation, ultimately predisposing the heart to failure. Krüppel-like factors (KLFs) are transcriptional regulators implicated in cardiovascular development and disease; however, a comprehensive temporal characterization of their coordinated activity during post-injury remodeling remains lacking. Objective: To define the temporal orchestration of the KLF family during myocardial injury and hypertrophy, and to integrate these dynamics within regulatory networks associated with cardiac remodeling. Methods: Myocardial injury was induced in rats using intraperitoneal isoproterenol. Left ventricular tissue was collected over a 21-day period. Cardiac morphometry, histology, immunohistochemistry, and quantitative gene expression analyses were performed to evaluate structural and transcriptional changes. Publicly available human cardiac and fibroblast datasets were analyzed for translational comparison, and protein-protein interaction networks were constructed to identify functional associations. Results: Isoproterenol treatment induced progressive hypertrophy, structural disorganization, and sustained fibrotic remodeling. KLFs displayed coordinated, phase-specific regulation, characterized by early activation of inflammation-associated members, intermediate engagement of factors linked to transforming growth factor signaling and hypertrophy modulation, and late induction of regulators associated with apoptosis and scar formation. These temporal patterns paralleled changes in inflammatory mediators, cardiac transcription factors, and genes involved in electrical and calcium handling pathways. Human expression analyses supported tissue-specific specialization of key KLFs. Conclusions: KLFs exhibit a coordinated and temporally structured regulatory program during myocardial remodeling, functioning as a transcriptional network that integrates inflammation, fibrosis, hypertrophy, and electrical adaptation. These findings position KLFs as key regulatory nodes in cardiac remodeling and potential targets for therapeutic intervention.

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