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      Cardiovascular protection of YiyiFuzi powder and the potential mechanisms through modulating mitochondria-endoplasmic reticulum interactions

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          Abstract

          Cardiovascular diseases (CVD) remain the leading cause of death worldwide and represent a major public health challenge. YiyiFuzi Powder (YYFZ), composed of Coicis semen and Fuzi, is a classical traditional Chinese medicine prescription from the Synopsis of Golden Chamber dating back to the Han Dynasty. Historically, YYFZ has been used to treat various CVD, rooted in Chinese therapeutic principles. Network pharmacology analysis indicated that YYFZ may exhibit direct or indirect effects on mitochondria-endoplasmic reticulum (ER) interactions. This review, focusing on the cardiovascular protective effects of Coicis semen and Fuzi, summarizes the potential mechanisms by which YYFZ acts on mitochondria and the ER. The underlying mechanisms are associated with regulating cardiovascular risk factors (such as blood lipids and glucose), impacting mitochondrial structure and function, modulating ER stress, inhibiting oxidative stress, suppressing inflammatory responses, regulating cellular apoptosis, and maintaining calcium ion balance. The involved pathways include, but were not limited to, upregulating the IGF-1/PI3K/AKT, cAMP/PKA, eNOS/NO/cGMP/SIRT1, SIRT1/PGC-1α, Klotho/SIRT1, OXPHOS/ATP, PPARα/PGC-1α/SIRT3, AMPK/JNK, PTEN/PI3K/AKT, β2-AR/PI3K/AKT, and modified Q cycle signaling pathways. Meanwhile, the MCU, NF-κB, and JAK/STAT signaling pathways were downregulated. The PERK/eIF2α/ATF4/CHOP, PERK/SREBP-1c/FAS, IRE1, PINK1-dependent mitophagy, and AMPK/mTOR signaling pathways were bidirectionally regulated. High-quality experimental studies are needed to further elucidate the underlying mechanisms of YYFZ in CVD treatment.

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          PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes.

          Vamsi K Mootha, Cecilia M. Lindgren, Karl-Fredrik Eriksson … (2003)
          DNA microarrays can be used to identify gene expression changes characteristic of human disease. This is challenging, however, when relevant differences are subtle at the level of individual genes. We introduce an analytical strategy, Gene Set Enrichment Analysis, designed to detect modest but coordinate changes in the expression of groups of functionally related genes. Using this approach, we identify a set of genes involved in oxidative phosphorylation whose expression is coordinately decreased in human diabetic muscle. Expression of these genes is high at sites of insulin-mediated glucose disposal, activated by PGC-1alpha and correlated with total-body aerobic capacity. Our results associate this gene set with clinically important variation in human metabolism and illustrate the value of pathway relationships in the analysis of genomic profiling experiments.
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            The unfolded protein response: controlling cell fate decisions under ER stress and beyond.

            Claudio Hetz (2012)
            Protein-folding stress at the endoplasmic reticulum (ER) is a salient feature of specialized secretory cells and is also involved in the pathogenesis of many human diseases. ER stress is buffered by the activation of the unfolded protein response (UPR), a homeostatic signalling network that orchestrates the recovery of ER function, and failure to adapt to ER stress results in apoptosis. Progress in the field has provided insight into the regulatory mechanisms and signalling crosstalk of the three branches of the UPR, which are initiated by the stress sensors protein kinase RNA-like ER kinase (PERK), inositol-requiring protein 1α (IRE1α) and activating transcription factor 6 (ATF6). In addition, novel physiological outcomes of the UPR that are not directly related to protein-folding stress, such as innate immunity, metabolism and cell differentiation, have been revealed.
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              AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1alpha.

              Sibylle Jager, Christoph Handschin, Julie St-Pierre … (2007)
              Activation of AMP-activated kinase (AMPK) in skeletal muscle increases glucose uptake, fatty acid oxidation, and mitochondrial biogenesis by increasing gene expression in these pathways. However, the transcriptional components that are directly targeted by AMPK are still elusive. The peroxisome-proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) has emerged as a master regulator of mitochondrial biogenesis; furthermore, it has been shown that PGC-1alpha gene expression is induced by exercise and by chemical activation of AMPK in skeletal muscle. Using primary muscle cells and mice deficient in PGC-1alpha, we found that the effects of AMPK on gene expression of glucose transporter 4, mitochondrial genes, and PGC-1alpha itself are almost entirely dependent on the function of PGC-1alpha protein. Furthermore, AMPK phosphorylates PGC-1alpha directly both in vitro and in cells. These direct phosphorylations of the PGC-1alpha protein at threonine-177 and serine-538 are required for the PGC-1alpha-dependent induction of the PGC-1alpha promoter. These data indicate that AMPK phosphorylation of PGC-1alpha initiates many of the important gene regulatory functions of AMPK in skeletal muscle.
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                Author and article information

                Contributors
                Jingyi Ding: URI : https://loop.frontiersin.org/people/1335061/overviewRole: Role: Role: Role: Role: Role: Role: Role: Role:
                Ran Ji: URI : https://loop.frontiersin.org/people/2697319/overviewRole: Role: Role: Role: Role:
                Ziyi Wang: Role: Role: Role: Role:
                Yuzhi Jia: URI : https://loop.frontiersin.org/people/1845861/overviewRole: Role: Role: Role:
                Tiantian Meng: URI : https://loop.frontiersin.org/people/1779716/overviewRole: Role: Role: Role:
                Xinbin Song: URI : https://loop.frontiersin.org/people/1912111/overviewRole: Role: Role: Role:
                Jing Gao: URI : https://loop.frontiersin.org/people/1922123/overviewRole: Role: Role: Role:
                Qingyong He: URI : https://loop.frontiersin.org/people/1526701/overviewRole: Role: Role:
                Journal
                Journal ID (nlm-ta): Front Pharmacol
                Journal ID (iso-abbrev): Front Pharmacol
                Journal ID (publisher-id): Front. Pharmacol.
                Title: Frontiers in Pharmacology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1663-9812
                Publication date (Electronic): 24 June 2024
                Publication date Collection: 2024
                Volume: 15
                Electronic Location Identifier: 1405545
                Affiliations
                [1] 1 Department of Cardiology , Guang’anmen Hospital , China Academy of Chinese Medical Sciences , Beijing, China
                [2] 2 Department of Intensive Care Unit , Guang’anmen Hospital , China Academy of Chinese Medical Sciences , Beijing, China
                [3] 3 Department of Rehabilitation , Dongfang Hospital , Beijing University of Chinese Medicine , Beijing, China
                [4] 4 Graduate School , Henan University of Chinese Medicine , Zhengzhou, China
                Author notes

                Edited by: Kroekkiat Chinda, Naresuan University, Thailand

                Reviewed by: Kai Yang, Shandong University of Traditional Chinese Medicine, China

                Peizheng Yan, Shandong University of Traditional Chinese Medicine, China

                Pingjun Zhu, People’s Liberation Army General Hospital, China

                *Correspondence: Qingyong He, heqingyongg@ 123456163.com
                [ † ]

                These authors have contributed equally to this work and share first authorship

                Article
                Publisher ID: 1405545
                DOI: 10.3389/fphar.2024.1405545
                PMC ID: 11228702
                PubMed ID: 38978978
                SO-VID: c91a0475-a4bd-455b-9628-5733bb7941a1
                Copyright © Copyright © 2024 Ding, Ji, Wang, Jia, Meng, Song, Gao and He.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 23 March 2024
                Date accepted : 28 May 2024
                Funding
                The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was financially supported by the Traditional Chinese Medicine Ancient Book Documents and Characteristic Technology Inheritance Project of the National Administration of Traditional Chinese Medicine (GZY-KJS-2020-079) and Research and Transformation Application of Clinical Characteristic Diagnosis and Treatment Techniques in the Capital (Z221100007422081).
                Categories
                Subject: Pharmacology
                Subject: Review
                Custom metadata
                section-at-acceptance Ethnopharmacology

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cardiovascular disease,mitochondria,endoplasmic reticulum,chinese herbal medicine,yiyifuzi powder
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cardiovascular disease, mitochondria, endoplasmic reticulum, chinese herbal medicine, yiyifuzi powder

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