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Article

Targeting PDK4 attenuates neointimal hyperplasia and regulates VSMC phenotypic switching, apoptosis, and autophagy.

Biochemical pharmacology - 1 May 2026

Sarkar Ankan, Ahmed Sakeel, Singh Monika, Zargar Zahid Bashir, Pawar Sandip V, Sharma Shyam Sunder, Chopra Kanwaljit, Jain Manish

Abstract excerpt

Neointimal hyperplasia, a predominant cause of restenosis and atherosclerosis, is regulated by the phenotypic modulation, migration and proliferation, of vascular smooth muscle cells (VSMCs). Pyruvate dehydrogenase kinase 4 (PDK4) has been identified as a key metabolic regulator linked to cancer cell proliferation. However, the specific mechanistic role of PDK4 in VSMC function and neointimal formation remains...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 41687829
DOI: 10.1016/j.bcp.2026.117805

Genes

PDK4
ATG7
BAX
LAMP1
MMP2
MMP9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

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Targeting PDK4 attenuates neointimal hyperplasia and regulates VSMC phenotypic switching, apoptosis, and autophagy.PMID 41687829Read ↗

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