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Recent Advances in Apoptosis and Autophagy
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Recent Advances in Apoptosis and Autophagy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (28 February 2024) | Viewed by 3768

Special Issue Editors

Dr. Alessandra Stacchiotti

E-Mail Website
Guest Editor
1. Dipartimento di Scienze Biomediche per la Salute, Università degli Studi di Milano, 20133 Milan, Italy
2. U.O. Laboratorio di Morfologia Applicata, IRRCS Policlinico San Donato, 20097 San Donato Milanese, Italy
Interests: autophagy; mitophagy; ER stress; apoptosis; metabolic diseases; cardiovascular diseases; mitochondria; antioxidants; microscopy; translational models of metabolic diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Annalisa Cappella

E-Mail Website
Guest Editor
1. Dipartimento di Scienze Biomediche per la Salute, Università degli Studi di Milano, 20133 Milan, Italy
2. U.O. Laboratorio di Morfologia Applicata, IRRCS Policlinico San Donato, 20097 San Donato Milanese, Italy
Interests: autophagy; mitophagy; apoptosis; skeletal system; bone tissue; healing process; skeletal diseases; role of antioxidants, aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cell loss and the progressive deterioration of organ and tissue function are among the main causes of aging-associated and autoimmune diseases. Autophagy and apoptosis are well-known conserved processes involved in cellular and tissue dismantling and renovation, and a proper cellular balance allows for the maintenance of health. However, the interdependence between these pivotal processes is still debated: does one activate or suppress the other? The formerly morphological classification of three types of programmed cell death, i.e., type I—apoptosis; type II—autophagy; and type III—necrosis, is now outdated. Different death mechanisms linked to aberrant metabolism; ischemia; inflammation; oncogenesis, called anoikis; efferocytosis; pyroptosis; and ferroptosis have emerged. In this complex scenery, molecular pathways based on caspase enzymes, receptor-interacting serine/threonine-protein kinase 1-3 (RIPK1-3), glutathione peroxidase 4 (GPX4) and the mechanistic target of rapamycin kinase (mTOR) play a crucial role. The constant exchange of knowledge between clinical and biological researchers regarding programmed cell death pathways and the use of natural or synthetic modulators of apoptosis (and related efferocytosis) and autophagy may lead to novel therapeutic opportunities.

To address the most recent advances in autophagy, apoptosis, and other cell death mechanisms in aging-related disorders, we are proposing this Special Issue that welcomes original articles, comprehensive reviews and/or perspective articles.

Dr. Alessandra Stacchiotti
Dr. Annalisa Cappella
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • efferocytosis
  • apoptosis
  • autophagy
  • mitophagy
  • cell death mechanisms
  • aging
  • cardiovascular diseases
  • musculoskeletal diseases
  • nutraceutical and natural modulators

Published Papers (2 papers)

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Research

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19 pages, 3760 KiB  
Article
Cardiometabolic Changes in Sirtuin1-Heterozygous Mice on High-Fat Diet and Melatonin Supplementation
by Gaia Favero, Igor Golic, Francesca Arnaboldi, Annalisa Cappella, Aleksandra Korac, Maria Monsalve, Alessandra Stacchiotti and Rita Rezzani
Int. J. Mol. Sci. 2024, 25(2), 860; https://doi.org/10.3390/ijms25020860 - 10 Jan 2024
Viewed by 1347
Abstract
A hypercaloric fatty diet predisposes an individual to metabolic syndrome and cardiovascular complications. Sirtuin1 (SIRT1) belongs to the class III histone deacetylase family and sustains anabolism, mitochondrial biogenesis, and fat distribution. Epididymal white adipose tissue (eWAT) is involved in inflammation, whilst interscapular brown [...] Read more.
A hypercaloric fatty diet predisposes an individual to metabolic syndrome and cardiovascular complications. Sirtuin1 (SIRT1) belongs to the class III histone deacetylase family and sustains anabolism, mitochondrial biogenesis, and fat distribution. Epididymal white adipose tissue (eWAT) is involved in inflammation, whilst interscapular brown adipose tissue (iBAT) drives metabolism in obese rodents. Melatonin, a pineal indoleamine, acting as a SIRT1 modulator, may alleviate cardiometabolic damage. In the present study, we morphologically characterized the heart, eWAT, and iBAT in male heterozygous SIRT1+/− mice (HET mice) on a high-fat diet (60%E lard) versus a standard rodent diet (8.5% E fat) and drinking melatonin (10 mg/kg) for 16 weeks. Wild-type (WT) male C57Bl6/J mice were similarly fed for comparison. Cardiomyocyte fibrosis and endoplasmic reticulum (ER) stress response worsened in HET mice on a high-fat diet vs. other groups. Lipid peroxidation, ER, and mitochondrial stress were assessed by 4 hydroxy-2-nonenal (4HNE), glucose-regulated protein78 (GRP78), CCAA/enhancer-binding protein homologous protein (CHOP), heat shock protein 60 (HSP60), and mitofusin2 immunostainings. Ultrastructural analysis indicated the prevalence of atypical inter-myofibrillar mitochondria with short, misaligned cristae in HET mice on a lard diet despite melatonin supplementation. Abnormal eWAT adipocytes, crown-like inflammatory structures, tumor necrosis factor alpha (TNFα), and iBAT whitening characterized HET mice on a hypercaloric fatty diet and were maintained after melatonin supply. All these data suggest that melatonin’s mechanism of action is strictly linked to full SIRT1 expression, which is required for the exhibition of effective antioxidant and anti-inflammatory properties. Full article
(This article belongs to the Special Issue Recent Advances in Apoptosis and Autophagy)
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Review

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21 pages, 5081 KiB  
Review
Influence of DNA Methylation on Vascular Smooth Muscle Cell Phenotypic Switching
by Chanthong Yorn, Hyunjung Kim and Kyuho Jeong
Int. J. Mol. Sci. 2024, 25(6), 3136; https://doi.org/10.3390/ijms25063136 - 8 Mar 2024
Viewed by 1841
Abstract
Vascular smooth muscle cells (VSMCs) are crucial components of the arterial wall, controlling blood flow and pressure by contracting and relaxing the artery walls. VSMCs can switch from a contractile to a synthetic state, leading to increased proliferation and migratory potential. Epigenetic pathways, [...] Read more.
Vascular smooth muscle cells (VSMCs) are crucial components of the arterial wall, controlling blood flow and pressure by contracting and relaxing the artery walls. VSMCs can switch from a contractile to a synthetic state, leading to increased proliferation and migratory potential. Epigenetic pathways, including DNA methylation, play a crucial role in regulating VSMC differentiation and phenotypic flexibility. DNA methylation involves attaching a methyl group to the 5’ carbon of a cytosine base, which regulates gene expression by interacting with transcription factors. Understanding the key factors influencing VSMC plasticity may help to identify new target molecules for the development of innovative drugs to treat various vascular diseases. This review focuses on DNA methylation pathways in VSMCs, summarizing mechanisms involved in controlling vascular remodeling, which can significantly enhance our understanding of related mechanisms and provide promising therapeutic approaches for complex and multifactorial diseases. Full article
(This article belongs to the Special Issue Recent Advances in Apoptosis and Autophagy)
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