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Life
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Alterations of the Metabolic Homeostasis in Aging
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Alterations of the Metabolic Homeostasis in Aging

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (30 August 2024) | Viewed by 3899

Special Issue Editor

Dr. Ji Li

E-Mail Website
Guest Editor
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA
Interests: AMPK signal transduction; heart failure; cancer; energy metabolism; aging; Alzheimer’s disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is critical to elucidate molecular and physiological mechanisms by which metabolic homeostasis is altered with aging in order to improve therapeutic strategies for the elderly. Accumulating evidence suggests that an age-related impairment is postulated to be a mechanism for a decline in stress tolerance observed with aging. In addition, significant progress has been made by demonstrating that metabolic homeostasis and inflammatory response play key roles in age-related cardiovascular and neurovascular diseases and cancer. Identifying good pharmacological approaches on these age-related diseases is an unmet need in the biomedical research field to prevent, delay or reverse the age-related impairments. This Special Issue of Life welcomes all related research papers and review articles associated with age-related diseases.

Dr. Ji Li
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • aging
  • cardiovascular impairment
  • neurodegenerative disease
  • cancer
  • metabolic homeostasis
  • inflammatory response

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Published Papers (2 papers)

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Research

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19 pages, 2103 KiB  
Article
Plasma Proteomics of Type 2 Diabetes, Hypertension, and Co-Existing Diabetes/Hypertension in Thai Adults
by Puriwat Fakfum, Hataichanok Chuljerm, Wason Parklak, Sittiruk Roytrakul, Narumon Phaonakrop, Peerasak Lerttrakarnnon and Kanokwan Kulprachakarn
Life 2024, 14(10), 1269; https://doi.org/10.3390/life14101269 - 5 Oct 2024
Cited by 1 | Viewed by 1554
Abstract
The study explored proteomics to better understand the relationship between type 2 diabetes (T2DM) and hypertension (HT) in Thai adults, using shotgun proteomics and bioinformatics analysis. Plasma samples were taken from 61 subjects: 14 healthy subjects (mean age = 40.85 ± 7.12), 13 [...] Read more.
The study explored proteomics to better understand the relationship between type 2 diabetes (T2DM) and hypertension (HT) in Thai adults, using shotgun proteomics and bioinformatics analysis. Plasma samples were taken from 61 subjects: 14 healthy subjects (mean age = 40.85 ± 7.12), 13 with T2DM (mean age = 57.38 ± 6.03), 16 with HT (mean age = 66.87 ± 10.09), and 18 with coexisting T2DM/HT (mean age = 58.22 ± 10.65). Proteins were identified using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Protein–protein interactions were analyzed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) version 11.5. We identified six unique proteins in T2DM patients, including translationally controlled 1 (TPT1) and nibrin (NBN), which are associated with the DNA damage response. In HT patients, seven unique proteins were identified, among them long-chain fatty acid-CoA ligase (ASCL), which functions in the stimulation of triacylglycerol and cholesterol synthesis, and NADPH oxidase activator 1 (NOXA1), which is involved in high blood pressure via angiotensin II-induced reactive oxygen species (ROS)-generating systems. In coexisting T2DM/HT patients, six unique proteins were identified, of which two—microtubule-associated protein 1A (MAP1A)—might be involved in dementia via RhoB-p53 and diacylglycerol kinase beta (DGKB), associated with lipid metabolism. This study identified new candidate proteins that are possibly involved in the pathology of these diseases. Full article
(This article belongs to the Special Issue Alterations of the Metabolic Homeostasis in Aging)
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Review

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14 pages, 735 KiB  
Review
Myeloid Cells in Myocardial Ischemic Injury: The Role of the Macrophage Migration Inhibitory Factor
by Hao Wang, Nadiyeh Rouhi, Lily A. Slotabec, Blaise C. Seale, Changhong Wen, Fernanda Filho, Michael I. Adenawoola and Ji Li
Life 2024, 14(8), 981; https://doi.org/10.3390/life14080981 - 5 Aug 2024
Viewed by 1893
Abstract
Ischemic heart disease, manifesting as myocardial infarction (MI), remains the leading cause of death in the western world. Both ischemia and reperfusion (I/R) cause myocardial injury and result in cardiac inflammatory responses. This sterile inflammation in the myocardium consists of multiple phases, involving [...] Read more.
Ischemic heart disease, manifesting as myocardial infarction (MI), remains the leading cause of death in the western world. Both ischemia and reperfusion (I/R) cause myocardial injury and result in cardiac inflammatory responses. This sterile inflammation in the myocardium consists of multiple phases, involving cell death, tissue remodeling, healing, and scar formation, modulated by various cytokines, including the macrophage migration inhibitory factor (MIF). Meanwhile, different immune cells participate in these phases, with myeloid cells acting as first responders. They migrate to the injured myocardium and regulate the initial phase of inflammation. The MIF modulates the acute inflammatory response by affecting the metabolic profile and activity of myeloid cells. This review summarizes the role of the MIF in regulating myeloid cell subsets in MI and I/R injury and discusses emerging evidence of metabolism-directed cellular inflammatory responses. Based on the multifaceted role of the MIF affecting myeloid cells in MI or I/R, the MIF can be a therapeutic target to achieve metabolic balance under pathology and alleviate inflammation in the heart. Full article
(This article belongs to the Special Issue Alterations of the Metabolic Homeostasis in Aging)
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