ArticleFrontiers in cardiovascular medicine2021
Pilose Antler Peptide-3.2KD Ameliorates Adriamycin-Induced Myocardial Injury Through TGF-β/SMAD Signaling Pathway.
Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 14 citations in OpenAlex.
- Deer antler polypeptides promote osteogenesis for fracture healing via activating neurosensory PGE2/EP4/p-CREB axis.Journal of orthopaedic translation · 2026Article
- Traditional Chinese medicine-induced cardiac adverse reactions: a critical review of current evidence, knowledge gaps, and pharmacovigilance strategies.Frontiers in pharmacology · 2026Review
- Role of BMP-7 in Cardiovascular Diseases: From Molecular Mechanisms to Therapeutic Horizons.Current drug targets · 2026Review
- Modern Advances in Velvet Antler Research: From Identification Methods to Pharmacological Mechanisms.International journal of food science · 2026Review
- Early treatment with nootkatone prevents pressure overload-induced ventricular remodeling and heart failure.Frontiers in pharmacology · 2025Article
- Well-known polypeptides of deer antler velvet with key actives: modern pharmacological advances.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Angiotensin-(1-9) attenuates adriamycin-induced cardiomyopathy in rats via the angiotensin type 2 receptor.Molecular and cellular biochemistry · 2024Article
- Effect of Tuina along "bladder meridian" alleviating intervertebral disc degeneration by regulating the transforming growth factor-β1/Smad signaling pathway in a rabbit model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- The recent progress of peptide regulators for the Wnt/β-catenin signaling pathway.Frontiers in medicine · 2023Review
- Health Effects of Peptides Extracted from Deer Antler.Nutrients · 2022Review
- The Protective Effect of Pilose Antler Peptide on CUMS-Induced Depression Through AMPK/Sirt1/NF-κB/NLRP3-Mediated Pyroptosis.Frontiers in pharmacology · 2022Article
- MiR-410-3p facilitates Angiotensin II-induced cardiac hypertrophy by targeting Smad7.Bioengineered · 2022Article
- Role and molecular mechanism of traditional Chinese medicine in preventing cardiotoxicity associated with chemoradiotherapy.Frontiers in cardiovascular medicine · 2022Review
- Shexiang Tongxin Dropping Pill Protects Against Chronic Heart Failure in MiceFrontiers in pharmacology · 2021Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adriamycin (ADR)-based combination chemotherapy is the standard treatment for some patients with tumors in clinical, however, long-term application can cause dose-dependent cardiotoxicity. Pilose Antler, as a traditional Chinese medicine, first appeared in the Han Dynasty and has been used to treat heart disease for nearly a thousand years. Previous data revealed pilose antler polypeptide (PAP, 3.2KD) was one of its main active components with multiple biological activities for cardiomyopathy. PAP-3.2KD exerts protective effects againt myocardial fibrosis. The present study demonstrated the protective mechanism of PAP-3.2KD against Adriamycin (ADR)-induced myocardial injury through using animal model with ADR-induced myocardial injury. PAP-3.2KD markedly improved the weight increase and decreased the HW/BW index, heart rate, and ST height in ADR-induced groups. Additionally, PAP-3.2KD reversed histopathological changes (such as disordered muscle bundles, myocardial fibrosis and diffuse myocardial cellular edema) and scores of the heart tissue, ameliorated the myocardial fibrosis and collagen volume fraction through pathological examination, significantly increased the protein level of Bcl-2, and decreased the expression levels of Bax and caspase-3 in myocardial tissue by ELISA, compared to those in ADR-induced group. Furthermore, ADR stimulation induced the increased protein levels of TGF-β1 and SMAD2/3/4, the increased phosphorylation levels of SMAD2/3 and the reduced protein levels of SMAD7. The expression levels of protein above in ADR-induced group were remarkably reversed in PAP-3.2KD-treated groups. PAP-3.2KD ameliorated ADR-induced myocardial injury by regulating the TGF-β/SMAD signaling pathway. Thus, these results provide a strong rationale for the protective effects of PAP against ADR-induced myocardial injury, when ADR is used to treat cancer.
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