Senescence-Associated Secretory Phenotype of Cardiovascular System Cells and Inflammaging: Perspectives of Peptide Regulation.

Khavinson V, Linkova N, Dyatlova A, Kantemirova R, Kozlov K. Cells. 2022.

Organ: vascular-cardiac · Type: review · Peptides: KED, AEDR

PMID: 36611900

An open-access 2022 review of SASP and inflammaging in cardiovascular cells, naming KED and AEDR among peptides proposed to touch those pathways — a perspective piece, not a trial.

Editorial summary of a 2022 Cells review (MDPI, open access: doi:10.3390/cells12010106). Public pages cite PubMed; the DOI is the OA record. Read the paper: PMID 36611900.

Methods

Narrative review. The authors collect signaling molecules that form the senescence-associated secretory phenotype (SASP) and inflammaging in cardiovascular-system cells, then survey peptides proposed to act on those molecules. No new patient cohort or cell assay is generated here.

Findings

The authors characterize cardiovascular SASP as altered anti-proliferative proteins (p16, p19, p21, p38, p53), inflammaging cytokines (IL-1α/β, IL-4, IL-6, IL-8, IL-18, TNFα, TGFβ1, NF-κB, MCP), matrix metalloproteinases, adhesion molecules, and sirtuins. They argue that vasoprotective polypeptides (they list liraglutide, atrial natriuretic peptide, and mimetics of relaxin, Ucn1, and adropin), the tripeptide KED, and the tetrapeptide AEDR regulate synthesis of molecules involved in inflammaging and SASP in cardiovascular cells, and that this is a rationale for peptide-based drugs in age-associated cardiovascular disease.

That is a mechanistic perspective built from prior papers. The review does not show that KED or AEDR treat atherosclerosis, coronary disease, or infarction. Follow the PMID and the OA DOI.