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Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism (2nd Edition)
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Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism (2nd Edition)

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 15 February 2026 | Viewed by 2643

Special Issue Editor

Prof. Dr. Vishwanath Venketaraman

E-Mail Website
Guest Editor
Microbiology/Immunology Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766-1854, USA
Interests: mycobacterial diseases; tuberculosis; host immune responses; pathogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immunologists have long been puzzled by the self-destructive nature of the inflammatory response. Inflammation can be elicited by various harmful stimuli, such as microbial/viral infections, allergic reactions, chemical insults, lipotoxicity, tissue damage, or other traumas. Breaking down damaged cells and converting them into various nutrients for tissue regeneration is one of the most important functions of the human immune system to maintain health. A localized inflammatory response is protective if the human immune system can effectively eliminate harmful stimuli and initiate healing. Cell self-destruction (programmed cell death) includes apoptosis, pyroptosis, necroptosis, necrosis, etc. Phagocytosis removes various cell debris produced by cell self-destruction and converts these debris into nutrients. The immune system thus becomes a powerful nutrient generator. At this time, digestion and immunity are interrelated and integrated and play the essential role of disease prevention and immunonutrition acquisition. In the event of microbial/viral infections, the nutritional flux produced by infected host cell self-destruction (inflammation) may be much greater than those produced by normal apoptosis and much greater than the nutrition provided by daily food intake. Thus, infection-induced inflammation may induce illness-associated anorexia to avoid overnutrition. When the nutrition generated by the degradation of infection-damaged cells exceeds the nutritional requirements of tissue regeneration, most of the excess nutrients will be converted into lipid intermediates. Lipid intermediates will invade healthy non-adipose tissue, leading to lipotoxicity and further tissue damage. In such a case, the inflammatory response's main product (lipid intermediates) is also a strong harming stimuli for tissue/cell damage, amplified during the inflammatory response, forming a vicious cycle, making the inflammatory response extremely destructive. The state of overnutrition will be exacerbated by the loss of lean body mass, coupled with excess lipid intermediates spillover into healthy tissues and organs, exacerbating the inflammatory response, which is characteristic of critically ill or injured patients and in most autoimmune diseases.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: microbial/viral infection-induced host cell self-destruction as immunonutrition; programmed cell death and nutrient generation; and cell self-destruction in illness, transient over-nutrition, lipotoxicity, and involuntary weight loss.

Prof. Dr. Vishwanath Venketaraman
Guest Editor

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. Biology 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 2700 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

  • autoimmunity
  • cell self-destruction
  • infection
  • inflammation
  • immunonutrition
  • lipotoxicity
  • metabolism
  • programmed cell death

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Related Special Issue

Published Papers (2 papers)

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Review

23 pages, 2759 KB  
Review
The Role of Mitochondrial Dysfunction and Dynamics in Hypertensive Heart Disease: Mechanisms and Recent Advances
by Bislom C. Mweene, Hanzooma Hatwiko, Joreen P. Povia and Sepiso K. Masenga
Biology 2025, 14(9), 1212; https://doi.org/10.3390/biology14091212 - 8 Sep 2025
Viewed by 748
Abstract
Hypertensive heart disease (HHD) is characterized by pressure overload-induced cardiac remodeling, in which mitochondrial dysfunction has emerged as a central contributor to pathophysiology. Mitochondria occupy roughly one-third of the volume of a cardiomyocyte and serve as the primary source of ATP for the [...] Read more.
Hypertensive heart disease (HHD) is characterized by pressure overload-induced cardiac remodeling, in which mitochondrial dysfunction has emerged as a central contributor to pathophysiology. Mitochondria occupy roughly one-third of the volume of a cardiomyocyte and serve as the primary source of ATP for the constantly active heart, while also regulating calcium homeostasis, redox balance, and apoptotic signaling. Chronic hypertension imposes energetic and oxidative stress on cardiomyocytes, disrupting mitochondrial structure and function. Key mitochondrial quality control processes including organelle fusion–fission dynamics, biogenesis, and mitophagy become dysregulated in HHD, leading to impaired energy production and heightened cell injury. This unstructured review discusses the physiological roles of mitochondria in cardiac muscle and examines how altered mitochondrial dynamics contribute to hypertensive cardiac damage. We detail mechanisms of mitochondrial dysfunction in HHD, such as excessive fission, cristae disruption, and oxidative stress, and how these changes are exacerbated by aging. Age-related mitochondrial remodeling such as loss of cristae and decreased organelle volume may synergistically worsen hypertensive cardiac injury. We further integrate findings from recent studies in animal and human models, including advanced three-dimensional ultrastructural analyses and molecular investigations that illuminate new aspects of mitochondrial network organization, the mitochondrial contact site and cristae organizing system (MICOS), cristae maintenance complex, and quality control pathways in HHD. Understanding mitochondrial dysfunction in HHD reveals potential therapeutic avenues targeting mitochondrial quality and dynamics to preserve cardiac function in hypertension. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism (2nd Edition))
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17 pages, 265 KB  
Review
New Advances in the Development and Design of Mycobacterium tuberculosis Vaccines: Construction and Validation of Multi-Epitope Vaccines for Tuberculosis Prevention
by Osnat Barazani, Thomas Erdos, Raafi Chowdhury, Gursimratpreet Kaur and Vishwanath Venketaraman
Biology 2025, 14(4), 417; https://doi.org/10.3390/biology14040417 - 13 Apr 2025
Cited by 1 | Viewed by 1609
Abstract
Mycobacterium tuberculosis (Mtb) vaccines are designed to prevent infection, prevent reactivation of latent infection, and/or provide adjuvant therapy to standard TB treatment for active Mtb. Emerging vaccine technologies include reverse vaccinology, DNA and RNA vaccines, subunit vaccines, and multi-epitope vaccines. Currently, many different [...] Read more.
Mycobacterium tuberculosis (Mtb) vaccines are designed to prevent infection, prevent reactivation of latent infection, and/or provide adjuvant therapy to standard TB treatment for active Mtb. Emerging vaccine technologies include reverse vaccinology, DNA and RNA vaccines, subunit vaccines, and multi-epitope vaccines. Currently, many different types of vaccine candidates are in clinical trials, though, to date, BCG remains the only approved Mtb vaccine. Mtb has a complex genome with numerous antigens, but not all are equally effective in eliciting immunity, so a critical challenge is the selection of antigens and epitopes that are most likely to induce a long-term, broad-spectrum protective immune response. Multi-epitope vaccines (MEVs) represent a new event horizon in vaccine development. Bioinformatic computer modeling is being used to maximize efficacy and minimalize adverse effects. Although no multi-epitope vaccines have proceeded to in vivo clinical trials, three candidate MEVs have made it through in silico tests. Multi-epitope vaccine candidate PP13138R, containing 13 HTL epitopes, 13 CTL epitopes, and 8 B cell epitopes in addition to both TLR2 and TLR4 agonists, aims to elicit a broad immune response that could address both active and latent Mtb infection. Similarly, immunoinformatic data were used to design and validate another MEV candidate based on the biomarker PE_PGRS17 with four B cell, nine HTL, and six CTL linked epitopes, with a griselimycin sequence as the adjuvant. A third novel prophylactic and therapeutic MEV was developed that targets Ag85A, AG85B, ESAT-6, and CFP-10 proteins with 12 CTL, 25 HTL, and 21 LBL epitopes with a CpG adjuvant. Full article
(This article belongs to the Special Issue Cell Self-Destruction (Programmed Cell Death), Immunonutrition and Metabolism (2nd Edition))
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