Review of PDGF-BB in aging-related diseases and proposed therapies
This review describes how PDGF-BB expression varies with natural aging and across cardiovascular, neurodegenerative, musculoskeletal and malignant diseases, and evaluates small molecules, natural products and biological agents that modulate PDGF-BB signaling as proposed targets for aging-related disorders. [1]
Automatic summary · not editorially reviewed
The key findings
The review reports that PDGF-BB expression varies markedly in time and place during natural aging and across cardiovascular, neurodegenerative, musculoskeletal and malignant diseases. [1]
PDGF-BB is described as acting through ERK, JNK, PI3K-AKT and mTOR pathways in a dose-dependent and cell-type-specific way. [1]
Small molecules, natural products and biological agents are reported to modulate PDGF-BB expression and downstream signaling, and the review evaluates their translational potential and limitations. [1]
The source at a glance
- Study type / format
- Narrative review (abstract only)
- Population / context
- Cells, tissues and disease contexts discussed in a review of PDGF-BB in natural aging and aging-related diseases
- Summary based on
- Study abstract
- Original publication
- September 22, 2026
PDGF-BB expression across aging and disease
According to the abstract, PDGF-BB is a core functional isoform of the PDGF family and a central regulator of cell proliferation, migration, differentiation and tissue remodeling. The review reports that its expression shows pronounced variation in time and place during natural aging and in cardiovascular, neurodegenerative and musculoskeletal diseases as well as malignancies. These expression patterns are described as linked to disease progression and distinct aging phenotypes. The abstract does not give specific expression values or name the tissues studied.
Supporting source [1]
Signaling pathways and dose-dependent effects
The abstract states that PDGF-BB starts complex intracellular signaling cascades, including the ERK, JNK, PI3K-AKT and mTOR pathways, by binding specific PDGFRα/β dimers. Through these networks it is said to coordinate communication between cells and to maintain the microenvironment in a highly dose-dependent and cell-type-specific manner. The review also describes a role in driving senescence and pathological progression. These are described mechanisms, not demonstrated human lifespan benefits.
Supporting source [1]
Proposed PDGF-BB-targeted therapies and open questions
The abstract reports that pharmacological interventions with small molecules, natural products and biological agents have shown efficacy in modulating PDGF-BB expression and its downstream signaling in preclinical and clinical evidence. It presents these as promising therapeutic targets for aging-related disorders and associated tissue damage. The review says it critically evaluates the translational potential and current limitations of such therapies and aims to provide a conceptual framework for future basic research and clinical translation. The abstract does not report specific agents, doses, outcomes or trial results.
Supporting source [1]
How to interpret this
This explainer is based only on the abstract; the full text was not reviewed. The abstract names no specific agents, doses, study designs, sample sizes, follow-up or outcome results, so the reported efficacy and therapeutic promise remain unquantified. Associations and described mechanisms do not establish that modulating PDGF-BB causes health or lifespan benefits in humans.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zheng M, Huang K, She Y, Qian J, Zhang F, Zhai Q. · europepmc.org · September 22, 2026