Aging and Metabolic Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (20 November 2025) | Viewed by 2842

Special Issue Editor


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Guest Editor
Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Ciudad Universitaria s/n, 28040 Madrid, Spain
Interests: mtorc1; autophagy; pancreatic beta cells; diabetes; mitophagy; tsc2; er-stress; MVB; exosomes; aging
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Special Issue Information

Dear Colleagues,

Different metabolic diseases, including T2DM and obesity, are two related and progressive diseases that represent a major public health problem in our modern society, contributing to alteration in the balance between a healthy situation and an unhealthy situation.  Both pathologies share several characteristics, including insulin resistance, hyperactivation of the mTORC1 signaling pathway, a low grade of inflammation, and an aged phenotype. One of the earliest pathophysiological features is insulin resistance, followed by a compensatory mechanism in pancreatic islets, which turns out to manifest hyperinsulinemia. The sustained secretion of pancreatic insulin constrains the incipient glucose intolerance in the second stage of type 2 diabetes progression. However, this compensatory mechanism finally fails, resulting in a full-blown phenotype. In addition to the changes previously mentioned, there are several alterations including mitochondrial dysfunction, dysfunctional autophagy, and an increase in oxidative stress. Different strategies have been studied in order to ameliorate all of these circumstances, such as calorie restriction, exercise, and intermittent fasting, among others, and could potentially modify the progression of the diseases, improving the free-disease period and potentiating a healthy life.

This Special Issue of Cells will highlight recent progress in aging and metabolic diseases through a collection of original research articles, reviews, and communications. We welcome all types of studies related to this topic to be submitted to this Special Issue.

Dr. Carlos Guillen
Guest Editor

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Keywords

  • aging
  • insulin resistance
  • diabetes
  • obesity
  • mitochondrial dysfunction
  • beta-galactosidase
  • senescent-associated secretory phenotype
  • pancreatic beta cells

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Published Papers (1 paper)

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Review

30 pages, 1911 KB  
Review
β-Cell Mitochondrial Dysfunction: Underlying Mechanisms and Potential Therapeutic Strategies
by Radwan Darwish, Yasmine Alcibahy, Ghena Abu-Sharia and Alexandra E. Butler
Cells 2025, 14(23), 1861; https://doi.org/10.3390/cells14231861 - 26 Nov 2025
Cited by 2 | Viewed by 2299
Abstract
Mitochondria are essential for β-cell function, coupling glucose metabolism to ATP production and insulin secretion. In diabetes, β-cell mitochondrial dysfunction arises from oxidative stress, impaired quality control and disrupted dynamics, leading to reduced oxidative phosphorylation, defective insulin release and progressive cell loss. Key [...] Read more.
Mitochondria are essential for β-cell function, coupling glucose metabolism to ATP production and insulin secretion. In diabetes, β-cell mitochondrial dysfunction arises from oxidative stress, impaired quality control and disrupted dynamics, leading to reduced oxidative phosphorylation, defective insulin release and progressive cell loss. Key transcriptional regulators link genetic susceptibility to mitochondrial dysfunction in both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). These disruptions impair mitophagy, mitochondrial translation and redox homeostasis. Therapeutic strategies that restore mitochondrial function, including mitophagy enhancers, mitochondrial antioxidants, and transcriptional regulators, have shown potential in preserving β-cell integrity. As mitochondrial failure precedes β-cell loss, targeting mitochondrial pathways may represent a critical approach to modifying diabetes progression. Full article
(This article belongs to the Special Issue Aging and Metabolic Diseases)
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