12/10/2026

MicroRNA as key players in skin regeneration and anti-aging pathways

Azizi et al.

For full text please see pdf.

05/10/2026

Glycemia reprograms substrate transport and shapes divergent stress responses in differentiating H9c2 cells

Passaponti et al.

For full text please see pdf.

07/08/2026

Stress management by benzodiazepines in septic shock and critical illness: mechanistic and clinical evidence supporting alternative sedative strategies

Lambertucci et al.

For full text please see pdf.

07/07/2026

Triptolide inhibits ovarian cancer growth and metastasis via reprogramming of tumor-associated macrophages

Chen et al.

For full text please see pdf.

03/07/2026

Polyamine-mediated inhibition of ferroptosis contributes to geroprotection

Madeo et al.

For full text please see pdf.

24/04/2026

The IRE1α-XBP1s-NFκB axis controls cell survival and epithelial differentiation under osmotic stress through arachidonic acid metabolism activation

Parra et al.

Arachidonic acid (AA) metabolism plays a critical role in renal cell osmoadaptation. We recently demonstrated that hypertonicity induces the expression and activation of cytosolic phospholipase A2 (cPLA2). On one hand, AA released by cPLA2 enhances triacylglyceride (TG) synthesis and accumulation. On the other hand, AA is converted into prostaglandins (PG) through cyclooxygenase 2 (COX2) activity. Both processes are required for renal cell survival under osmotic stress. However, the mechanisms by which hypertonicity induces cPLA2 expression remain poorly understood. Given that we previously shown that hypertonicity regulates TG synthesis through the IRE1α-XBP1s branch of the unfolded protein (…)

06/03/2026

Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential

Ebadollahibaruq et al.

This review meticulously dissects CNPY2’s structural characteristics, expression patterns, and biological functions across various disorders, emphasizing its role on tumor initiation, microenvironmental stress, and chemoresistance, and evaluating its potential as a therapeutic target.

30/01/2026

Antifungal peptides: from modes of action to synergistic and immunologic potential

Carmona-Gutierrez et al.
26/01/2026

Reversal of Cushing syndrome by antibody-mediated neutralization of ACBP/DBI

Shen et al.

For full text please see pdf.

17/01/2020

RPA and Pif1 cooperate to remove G-rich structures at both leading and lagging strand

Maestroni et al.

In Saccharomyces cerevisiae, the absence of Pif1 helicase induces the instability of G4-containing CEB1 minisatellite during leading strand but not lagging strand replication. We report that RPA and Pif1 cooperate to maintain CEB1 stability when the G4 forming strand is either on the leading or lagging strand templates. At the leading strand, RPA acts in the same pathway as Pif1 to maintain CEB1 stability. Consistent with this result, RPA co-precipitates with Pif1. This association between Pif1 and RPA is affected by the rfa1-D228Y mutation that lowers the affinity of RPA in particular for G-rich single-stranded DNA. At the lagging strand, in contrast to pif1∆, the rfa1-D228Y mutation strongly increases the frequency of CEB1 rearrangements. We explain that Pif1 is dispensable at the lagging strand DNA by the ability of RPA by itself to prevent formation of stable G-rich secondary structures during lagging (…)

14/10/2019

LTX-315 sequentially promotes lymphocyte-independent and lymphocyte-dependent antitumor effects

Liao et al.

LTX-315 is an oncolytic peptide that has antitumor efficacy in mice grafted with various tumor cell lines and is currently being tested in phase II clinical trials. Here we aimed to further evaluate LTX-315 in conditional genetic mouse models of cancer that typically resist current treatment options and to better understand the drug’s mode of action in vivo. We report LTX-315 mediates profound antitumor effects against Braf- and Pten-driven melanoma and delays the progression of Kras- and P53-driven soft tissue sarcoma in mice. Additionally, we show in melanoma that LTX-315 triggers two sequential phases of antitumor response. The first phase of response, which begins within minutes of drug delivery into tumors, is defined by disrupted tumor vasculature and decreased tumor burden and occurs independently of (…)

13/09/2019

Inflammation induced PD-L1-specific T cells

Munir et al.

PD-L1-specific T cells are a natural part of the T-cell repertoire in humans. Hence, we have previously described spontaneous CD8+ and CD4+ T-cell reactivity against PD-L1 in the peripheral blood of patients with various cancers as well as in healthy donors. It is well described that the expression of the PD-L1 protein is introduced in cells by pro-inflammatory cytokines, e.g. IFN-γ. In the current study, we were able to directly link inflammation with PD-L1-specific T cells by showing that inflammatory mediators such as IFN-γ generate measurable numbers of PD-L1-specific T cells in human PBMCs as well as in in vivo models. These PD-L1-specific T cells can vigorously modulate the cell compartments of the local environment. PD-L1-specific T cells may be important for immune homeostasis by sustaining the ongoing inflammatory response by the suppression of regulatory cell function both (…)

31/07/2019

Gold Nanoparticles sensitize pancreatic cancer cells to gemcitabine

Huai et al.

INTRODUCTION Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease. The mortality rate closely parallels that of incidence [1][2]. The current standard of care for advanced stage PDAC patients includes combination treatment with Nab-paclitaxel and

25/02/2019

The primary cilium protein folliculin is part of the autophagy signaling pathway to regulate epithelial cell size in response to fluid flow

Zemirli et al.

Autophagy is a conserved molecular pathway directly involved in the degradation and recycling of intracellular components. Autophagy is associated with a response to stress situations, such as nutrients deficit, chemical toxicity, mechanical stress or microbial host defense. We have recently shown that primary cilium-dependent autophagy is important to control kidney epithelial cell size in response to fluid flow induced shear stress. Here we show that the ciliary protein folliculin (FLCN) actively participates to the signaling cascade leading to the stimulation of fluid flow-dependent autophagy upstream of the cell size regulation in HK2 kidney epithelial cells. The knockdown of FLCN induces a shortening of the primary cilium, inhibits the activation of AMPK and the recruitment of the autophagy protein ATG16L1 at the primary cilium. Altogether, our results suggest that FLCN (…)

10/10/2018

p38β MAPK mediates ULK1-dependent induction of autophagy in skeletal muscle of tumor-bearing mice

Liu et al.

INTRODUCTION Cancer has been increasingly recognized as a systemic disorder that stresses multiple organs independent of its location. At least 50% of cancer patients experience cachexia, a systemic wasting syndrome manifested as weight loss, inflammation,

17/08/2018

Neuronal Lamin regulates motor circuit integrity and controls motor function and lifespan

Oyston et al.

Neuronal aging involves a progressive decline in cognitive abilities and loss of motor function. Mutations in human Lamin genes (LMNA, LMNB1, LMNB2) lead to a wide-range of diseases including muscular dystrophy, peripheral neuropathy and progeria. Here we investigate the role of neuronal Lamin in regulating age-related phenotypes. Neuronal targeting of Lamin led to shortened lifespan, progressive impairment of motor function and loss of dopaminergic (DA) neurons within the protocerebral anterior medial (PAM) cluster in the Drosophila melanogaster brain. Loss of neuronal Lamin caused an age-related decline in neural physiology, with slower neurotransmission and increased chance of motor circuit failure with age. Unexpectedly, Lamin-dependent decline in motor function was specific for the chemical synapses of the dorsal longitudinal muscle (DLM). Together (…)

21/03/2018

Assay for high-throughput screening of inhibitors of the ASC-PYD inflammasome core filament

Sborgi et al.

The protein ASC is a central component of most inflammasome complexes, forming functional oligomeric filaments that activate large amounts of pro-caspase-1 for further IL-1β processing and the induction of Gasdermin D-dependent cell death. The central role of inflammasomes in the innate immune response pose them as new molecular targets for therapy of diverse acute, chronic and inherited autoinflammatory pathologies. In recent years, an increasing number of molecules were proposed to modulate inflammasome signalling by interacting with different components of inflammasome complexes. However, the difficult in vitro reconstitution of the inflammasome has limited the development of specific on-target biochemical assays for compound activity confirmation and for drug discovery in high throughput screening setups. Here we describe a homogeneous, pH (…)

07/03/2018

Dram1 regulates DNA damage-induced alternative autophagy

Nagata et al.

Autophagy is an evolutionarily conserved process that degrades subcellular constituents. Mammalian cells undergo two types of autophagy; Atg5-dependent conventional autophagy and Atg5-independent alternative autophagy, and the molecules required for the latter type of autophagy are largely unknown. In this study, we analyzed the molecular mechanisms of genotoxic stress-induced alternative autophagy, and identified the essential role of p53 and damage-regulated autophagy modulator (Dram1). Dram1 was sufficient to induce alternative autophagy. In the mechanism of alternative autophagy, Dram1 functions in the closure of isolation membranes downstream of p53. These findings indicate that Dram1 plays a pivotal role in genotoxic stress-induced alternative autophagy.

12/12/2017

Targeting Nfix to fix muscular dystrophies

Rossi et al.

A shared knowledge in the field is that to be really successful, any therapeutic strategy has to rely on good muscle quality. In fact, there is no available approach able to rescue muscle damage when

05/12/2017

A game of substrates: replication fork remodeling and its roles in genome stability and chemo-resistance

Sidorova

During the hours that human cells spend in the DNA synthesis (S) phase of the cell cycle, they may encounter adversities such as DNA damage or shortage of nucleotides. Under these stresses, replication forks in DNA may experience slowing, stalling, and breakage. Fork remodeling mechanisms, which stabilize slow or stalled replication forks and ensure their ability to continue or resume replication, protect cells from genomic instability and carcinogenesis. Fork remodeling includes DNA strand exchanges that result in annealing of newly synthesized strands (fork reversal), controlled DNA resection, and cleavage of DNA strands. Defects in major tumor suppressor genes BRCA1 and BRCA2, and a subset of the Fanconi Anemia genes have been shown to result in deregulation in fork remodeling, and most prominently, loss of kilobases of nascent DNA from stalled replication forks. This phenomenon has recently gained spotlight as a potential marker and mediator of (…)

04/12/2017

New insight into the role of autophagy in tumorigenesis

Tian et al.

TP53, commonly known as p53, is an important tumor suppressor. Its increased expression was observed not only in the liver tumors of our Atg5-knockout mice but also in the lung tumors of Kras and Atg7

01/12/2017

Reciprocal regulatory circuits coordinating EMT plasticity

Diepenbruck and Christofori.

In the context of malignant tumor progression epithelial tumor cells can gain metastatic properties via an EMT induced by diverse extracellular stimuli (e.g. transforming growth factor β, TGFβ), which enables cancer cells to invade the

15/11/2017

Protein quality control meets transcriptome remodeling under stress

Mathew and Stirling

Protein quality control (PQC) is an essential part of cellular homeostasis and encompasses the balance of non-native protein folding and degradation. Under stress, triage of non-native or disassembled proteins to aggregate structures mitigates cellular damage

07/11/2017

Exploding the necroptotic bubble

Edry-Botzer and Gerlic

Several new types of regulated cell death have emerged from analysis of necrotic forms of cell death; one example is necroptosis, a RIPK3-MLKL-dependent and caspase-independent form of cell death. Although the initiation steps of necroptosis

02/10/2017

Emerging roles of mitochondria and autophagy in liver injury during sepsis

Aki et al.

Recent research indicates crucial roles of autophagy during sepsis. In animal models of sepsis induced by cecal ligation and puncture (CLP) or the systemic administration of lipopolysaccharides (LPS), autophagy is implicated in the activation and/or damage of various cells/organs, such as immune cells, heart, lung, kidney, and liver. Since sepsis is associated with an increased production of pro- as well as anti-inflammatory cytokines, it has long been considered that hypercytokinemia is a fetal immune response leading to multiple organ failure (MOF) and mortality of humans during sepsis. However, a recent paradigm illuminates the crucial roles of mitochondrial dysfunction as well as the perturbation of autophagy in the pathogenesis of sepsis. In the livers of animal models of sepsis, autophagy is involved in the elimination of damaged mitochondria to prevent the generation of mitochondrial ROS and the initiation of the mitochondrial apoptotic (…)

01/10/2017

Fumarase mediates transcriptional response to nutrient stress

Zhao and Jiang

To date, emerging evidence demonstrate that metabolites participate in a wide variety of cellular activities besides their direct role in metabolism. Previous studies have reported that metabolic activity of FH is critically involved in the

01/10/2017

VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress

Shoshan-Barmatz et al.

VDAC ISOFORMS, STRUCTURE, AND CHANNEL ACTIVITY VDAC isoforms and cellular localization Three different VDAC isoforms, VDAC1, VDAC2 and VDAC3, sharing ~70% identity and structural and some functional properties [cite]10.1016/j.mam.2010.03.002[/cite][cite]10.1016/j.bbamem.2011.10.005[/cite], are expressed in mammalian mitochondria, with

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21/11/2017

Metastatic-initiating cells and lipid metabolism

Aznar Benitah

INTRODUCTION Metastasis is an inefficient process at the cellular level, yet it is the leading cause of cancer-related deaths [cite]10.1016/j.stem.2014.02.002[/cite]. Despite intense investigation, the identity of the tumor cells with the capacity to colonize distant

01/11/2017

Tumor suppressive Ca2+ signaling is driven by IP3 receptor fitness

Bultynck and Campanella

Intracellular Ca2+ signals critically control a plethora of cellular functions, of which many impact cellular death and/or survival, processes often dysregulated in cancer [cite]10.1038/nrc.2017.18[/cite]. In healthy cells, Ca2+ signaling is employed for normal cell physiology

01/10/2017

The long non-coding RNA H19 – a new player in hepatocellular carcinoma

Ardelt and Pachmayr

Hepatocellular carcinoma (HCC) is among the most prevalent and lethal cancers worldwide [cite]10.3322/caac.20107[/cite]. Incidence is increasing and due to its high chemoresistance, the therapeutic options are limited and HCC has risen to become one of

01/10/2017

TFEB-mTORC1 feedback loop in metabolism and cancer

Di Malta and Ballabio

Everyday most organisms face the requirement to adapt their metabolic cues to the fluctuation of nutrient resources into the environment. When nutrients are abundant cells activate anabolic pathways, such as protein and lipid synthesis, and

01/10/2017

Cell Stress – a new journal for cellular pathophysiology

Zimmermann et al.

Any disease that humanity encounters is preceded by a homeostatic disruption as a prelude to a consequent pathological state. Medical researchers and practitioners try to counteract this by designing and optimizing appropriate diagnostic tools and

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FAQs

Whether you’re preparing a manuscript, reviewing a paper, or just exploring the journal, this FAQ answers the essentials—from scope and founders to impact and how to submit. Prefer a tailored path? Pick For authors or For reviewers below.

Peer-reviewed, open-access research using unicellular organisms (and multicellular microorganisms) to understand cellular responses and human disease.

The journal (founded in 2014) is led by its Editors-in-Chief Frank Madeo, Didac Carmona-Gutierrez, and Guido Kroemer

Microbial Cell has been publishing original scientific literature since 2014, and from the very beginning has been managed by active scientists through an independent Publishing House (Shared science Publishers). The journal was conceived as a platform to acknowledge the importance of unicellular organisms, both as model systems as well as in the biological context of human health and disease.

Ever since, Microbial Cell has very positively developed and strongly grown into a respected journal in the unicellular research community and even beyond. This scientific impact is reflected in the yearly number of citations obtained by articles published in Microbial Cell, as recorded by the Web of Science (Clarivate, formerly Thomson/Reuters):

The scientific impact of Microbial Cell is also mirrored in a series of milestones:

2015: Microbial Cell is included in the Emerging Sources Citation Index (ESCI), a selection of developing journals drafted by Clarivate Analytics based on the candidate’s publishing standards, quality, editorial content, and citation data. Note: As an ESCI-selected journal, Microbial Cell is currently being evaluated in a rigorous and long process to determine an inclusion in the Science Citation Index Expanded (SCIE), which allows the official calculation of Clarivate Analytics’ impact factor.

2016: Microbial Cell is awarded the so-called DOAJ Seal by the selective Directory of Open Access Journals (DOAJ). The DOAJ Seal is an exclusive mark of certification for open access journals granted by DOAJ to journals that adhere to outstanding best practice and achieve an extra high and clear commitment to open access and high publishing standards.

2017: Microbial Cell is included in Pubmed Central (PMC), allowing the archiving of all the journal’s articles in PMC and PubMed.

2019: Microbial Cell is indexed in the prestigious abstract and citation database Scopus after a thorough selection process. This also means that Microbial Cell obtains, for the first time, an official Scopus CiteScore as well as an official journal ranking in the Scimago Journal and Country Ranking.

2022: Microbial Cell’s CiteScore reaches a value of 7.2 for the year 2021, positioning Microbial Cell among the top microbiology journals (previously available CiteScores: 2019: 5.4; 2020: 5.1).

2022: Microbial Cell is indexed in the highly selective Science Citation Index Expanded™, which covers approx. 9,500 of the world’s most impactful journals across 178 scientific disciplines. In their journal selection and curation process, Clarivate´s editors apply 24 ‘quality’ criteria and four ‘impact’ criteria to select the most influential journals in their respective fields. This selection is also a pre-requisite for inclusion in the JCR, which features the impact factor.

2022: Microbial Cell is listed in the Journal Citation Reports™ (JCR), and obtains its first official Journal Impact Factor™ (JIF) for the year 2021: 5.316.

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