@article {6687,
	title = {Mindin (SPON2) Is Essential for Cutaneous Fibrogenesis in a Mouse Model of Systemic Sclerosis.},
	journal = {J Invest Dermatol},
	volume = {143},
	year = {2023},
	month = {2023 May},
	pages = {699-710.e10},
	abstract = {<p>Systemic sclerosis is a fibrotic disease that initiates in the skin and progresses to internal organs, leading to a poor prognosis. Unraveling the etiology of a chronic, multifactorial disease such as systemic sclerosis has been aided by various animal models that recapitulate certain aspects of the human pathology. We found that the transcription factor SNAI1 is overexpressed in the epidermis of patients with systemic sclerosis, and a transgenic mouse recapitulating this expression pattern is sufficient to induce many clinical features of the human disease. Using this mouse model as a discovery platform, we have uncovered a critical role for the matricellular protein Mindin (SPON2) in fibrogenesis. Mindin is produced by SNAI1 transgenic skin keratinocytes and aids fibrogenesis by inducing early inflammatory cytokine production and collagen secretion in resident dermal fibroblasts. Given the dispensability of Mindin in normal tissue physiology, targeting this protein holds promise as an effective therapy for fibrosis.</p>
},
	keywords = {Animals, Disease Models, Animal, Extracellular Matrix Proteins, Fibroblasts, Fibrosis, Humans, Mice, Mice, Transgenic, Neoplasm Proteins, Scleroderma, Systemic, Skin},
	issn = {1523-1747},
	doi = {10.1016/j.jid.2022.10.011},
	author = {Rana, Isha and Kataria, Sunny and Tan, Tuan Lin and Hajam, Edries Yousaf and Kashyap, Deepak Kumar and Saha, Dyuti and Ajnabi, Johan and Paul, Sayan and Jayappa, Shashank and Ananthan, Akhil S H P and Kumar, Pankaj and Zaarour, Rania F and Haarshaadri, J and Kansagara, Gaurav and Rizvi, Abrar and Zirmire, Ravindra K and Badarinath, Krithika and Khedkar, Sneha Uday and Chandra, Yogesh and Samuel, Rekha and George, Renu and Danda, Debashish and Jacob, Paul Mazhuvanchary and Dey, Rakesh and Dhandapany, Perundurai S and He, You-Wen and Varga, John and Varghese, Shyni and Jamora, Colin}
}
@article {2206,
	title = {Role of Hypoxia-Mediated Autophagy in Tumor Cell Death and Survival.},
	journal = {Cancers (Basel)},
	volume = {13},
	year = {2021},
	month = {2021 Jan 30},
	abstract = {<p>Programmed cell death or type I apoptosis has been extensively studied and its contribution to the pathogenesis of disease is well established. However, autophagy functions together with apoptosis to determine the overall fate of the cell. The cross talk between this active self-destruction process and apoptosis is quite complex and contradictory as well, but it is unquestionably decisive for cell survival or cell death. Autophagy can promote tumor suppression but also tumor growth by inducing cancer-cell development and proliferation. In this review, we will discuss how autophagy reprograms tumor cells in the context of tumor hypoxic stress. We will illustrate how autophagy acts as both a suppressor and a driver of tumorigenesis through tuning survival in a context dependent manner. We also shed light on the relationship between autophagy and immune response in this complex regulation. A better understanding of the autophagy mechanisms and pathways will undoubtedly ameliorate the design of therapeutics aimed at targeting autophagy for future cancer immunotherapies.</p>
},
	issn = {2072-6694},
	doi = {10.3390/cancers13030533},
	author = {Zaarour, Rania F and Azakir, Bilal and Hajam, Edries Y and Nawafleh, Husam and Zeinelabdin, Nagwa A and Engelsen, Agnete S T and Thiery, J{\'e}rome and Jamora, Colin and Chouaib, Salem}
}
