Examinando por Autor "Gómez, José"

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Low abundance of NDUFV2 and NDUFS4 subunits of the hydrophilic complex I domain and VDAC1 predicts mammalian longevity
(Elsevier, 2020-04-20) Mota-Martorell, Natalia; Jove, Mariona; Pradas, Irene; Sanchez, Isabel; Gómez, José; Naudi, Alba; Barja, Gustavo
Mitochondrial reactive oxygen species (ROS) production, specifically at complex I (Cx I), has been widely suggested to be one of the determinants of species longevity. The present study follows a comparative approach to analyse complex I in heart tissue from 8 mammalian species with a longevity ranging from 3.5 to 46 years. Gene expression and protein content of selected Cx I subunits were analysed using droplet digital PCR (ddPCR) and western blot, respectively. Our results demonstrate: 1) the existence of species-specific differences in gene expression and protein content of Cx I in relation to longevity; 2) the achievement of a longevity phenotype is associated with low protein abundance of subunits NDUFV2 and NDUFS4 from the matrix hydrophilic domain of Cx I; and 3) long-lived mammals show also lower levels of VDAC (voltage-dependent anion channel) amount. These differences could be associated with the lower mitochondrial ROS production and slower aging rate of long-lived animals and, unexpectedly, with a low content of the mitochondrial permeability transition pore in these species.
Mitochondrial ROS production, oxidative stress and aging within and between species: Evidences and recent advances on this aging effector
(Elsevier, 2023-02-27) Gómez, José; Mota-Martorell, Natália; Jové, Mariona; Pamplona, Reinald; Barja, Gustavo
Mitochondria play a wide diversity of roles in cell physiology and have a key functional implication in cell bioenergetics and biology of free radicals. As the main cellular source of oxygen radicals, mitochondria have been postulated as the mediators of the cellular decline associated with the biological aging. Recent evidences have shown that mitochondrial free radical production is a highly regulated mechanism contributing to the biological determination of longevity which is species-specific. This mitochondrial free radical generation rate induces a diversity of adaptive responses and derived molecular damage to cell components, highlighting mitochondrial DNA damage, with biological consequences that influence the rate of aging of a given animal species. In this review, we explore the idea that mitochondria play a fundamental role in the determination of animal longevity. Once the basic mechanisms are discerned, molecular approaches to counter aging may be designed and developed to prevent or reverse functional decline, and to modify longevity.
Programmed versus non-programmed evolution of aging. What is the evidence?
(Elsevier, 2023-04-05) Pamplona, Reinald; Jové, Mariona; Gómez, José; Barja, Gustavo
The evolutionary meaning and basic molecular mechanisms involved in the determination of longevity remain an unresolved problem. Currently, different theories are on offer in response to these biological traits and to explain the enormous range of longevities observed in the animal kingdom. These theories may be grouped into those that defend non-programmed aging (non-PA) and those that propose the existence of programmed aging (PA). In the present article we examine many observational and experimental data from both the field and from the laboratory and sound reasoning accumulated in recent decades both compatible and not with PA and non-PA evolutionary theories of aging. These analyses are briefly summarized and discussed. Our conclusion is that most of the data favour programmed aging with a possible contribution of non-PA antagonist pleiotropy in various cases.
Whole organism aging: Parabiosis, inflammaging, epigenetics, and peripheral and central aging clocks. The ARS of aging
(Elsevier, 2023-03-09) Pamplona, Reinald; Jové, Mariona; Gómez, José; Barja, Gustavo
The strong interest shown in the study of the causes of aging in recent decades has uncovered many mechanisms that could contribute to the rate of aging. These include mitochondrial ROS production, DNA modification and repair, lipid peroxidation-induced membrane fatty acid unsaturation, autophagy, telomere shortening rate, apoptosis, proteostasis, senescent cells, and most likely there are many others waiting to be discovered. However, all these well-known mechanisms work only or mainly at the cellular level. Although it is known that organs within a single individual do not age at exactly the same rate, there is a well-defined species longevity. Therefore, loose coordination of aging rate among the different cells and tissues is needed to ensure species lifespan. In this article we focus on less known extracellular, systemic, and whole organism level mechanisms that could loosely coordinate aging of the whole individual to keep it within the margins of its species longevity. We discuss heterochronic parabiosis experiments, systemic factors distributed through the vascular system like DAMPs, mitochondrial DNA and its fragments, TF-like vascular proteins, and inflammaging, as well as epigenetic and proposed aging clocks situated at different levels of organization from individual cells to the brain. These interorgan systems can help to determine species longevity as a further adaptation to the ecosystem.